FisiologíaBoletín informativo de la SECF • Volumen 23 - nº 2 • Diciembre 2020 ISSN: 1889-397X • TITULARES • • EDITORIAL • stimados amigos: TRPV2: AN ELUSIVE Antes de fin de año, como viene siendo PLAYER IN CENTRAL habitual, tenemos el placer de haceros llegar un nuevo ejemplar de la revista FISIOLOGÍA, que NERVOUS SYSTEM Een esta ocasión incorpora dos interesantes y PATHOPHYSIOLOGY estimulantes artículos. Jennifer Enrich-Bengoa andAlex Perálvarez-Marín. La primera de las revisiones, a cargo de Jennifer Enrich-Bengoa y Alex Perálvarez-Marín, del Departamento de Bioquímica y Biología Molecular de la GESTATIONAL DIABETES Universidad Autónoma de Barcelona, nos introduce en el papel del canal TRPV2 en la fisiología y la MELLITUSRISKIS fisiopatología del sistema nervioso central. Además de MEDIATED BY CHANGES una descripción del papel del canal en la función del sistema nervioso, así como su posible relación con IN THE CIRCULATING ciertas patologías, los autores mencionan distintos inhibidores farmacológicos del canal TRPV2 con un MICRORNAEXPRESSION potencial prometedor en la fisiopatología de PROFILE: UPDATES AND determinados desórdenes del sistema nervioso. PERSPECTIVES. La segunda de las revisiones, redactada por Paola Paola Pinto-Hernández, Cristina Tomás-Zapico and Eduardo Pinto-Hernández, Cristina Tomás-Zapico y Eduardo Iglesias-Gutiérrez. Iglesias-Gutiérrez, del Departamento de Biología Funcional de la Universidad de Oviedo, analiza los hallazgos recientes sobre el papel de los miRNA como biomarcadores de diabetes mellitus gestacional, sus LIBROSRECOMENDADOS actuales limitaciones y sus prometedoras perspectivas Fisiología Veterinaria de futuro basadas en su potencial valor diagnóstico y traslacional.

Esperamos que estos artículos resulten de vuestro agrado y que el año venidero sea amable con todos vosotros.

Juan A. Rosado • CALL FOR PAPERS • La revista Fisiología está buscando manuscritos relacionados con cualquiera de los aspectos básicos de la Fisiología celular, de tejidos, órganos y sistemas, incluyendo Fisiología humana, animal y comparada, así como aquellos dedicados al estudio de los desequilibrios de los procesos fisiológicos que dan como resultado alteraciones de la salud. Los autores deben enviar sus manuscritos al editor, Dr. Juan Antonio Rosado, vía correo electrónico a [email protected], incluyendo el texto del manuscrito y las figuras siguiendo el formato que se especifica en las instrucciones a los autores. Los manuscritos, que podrán estar redactados en español o inglés, serán revisados por el Comité Editorial, quienes podrán solicitar la opinión de expertos. Una vez aceptados, los manuscritos se publicarán en el primer volumen disponible. La revista Fisiología acepta manuscritos en los siguientes formatos: artículos originales, artículos de revisión, cartas, así como reseñas y comentarios sobre libros que versen sobre cualquiera de los aspectos relacionados con la Fisiología.

•Editor• Juan Antonio Rosado Dionisio. Departamento de Fisiología. Universidad de Extremadura. 10.003 Cáceres Teléfono: 927 25 71 39 • Fax: 927 25 71 10 • E-mail: [email protected] •Comité editorial• Diego Álvarez (Universidad de La Laguna, [email protected]),Teresa Giráldez (Universidad de La Laguna, [email protected]), Celestino González (Universidad de Oviedo, [email protected]), Ana Ilundain (Universidad de Sevilla, [email protected]), Juan Martínez-Pinna (Universidad de Alicante, [email protected]) y Carlos Villalobos (CSIC, [email protected]).

Diseño, Maquetación e Impresión: Imprema Gráficas Jardín S.L. - 927 62 63 89 - [email protected] SOCIEDAD ESPAÑOLA DE CIENCIAS FISIOLÓGICAS

• Presidenta: Meritxell López Gallardo ([email protected]) • Presidente Electo: Vicente Martínez Perea ([email protected]) • Presidente Saliente: Jorge García Seoane ([email protected]) • Secretaria: Eva María Marco López ([email protected])) • Tesorero: Antonio González Mateosz ([email protected]) • Vocales: Jesús Francisco Rodríguez Huertas ([email protected]) y María Inmaculada García Fernández ([email protected]). Direcciones de contacto en: http://www.secf.es/ · D.L.: SE-321-2000 • CARTA DE LA PRESIDENTA

ueridos amigos y queridos compañeros de la Sociedad Española de Ciencias Fisiológicas. Mi primera carta como Presidenta Ejecutiva solo puede comenzar con el deseo de que tanto vosotros como vuestras familias y amigos os encontréis bien. Agradezco que confiarais en mi para desarrollar esta labor, Q es un gran reto y, a la vez, un gran orgullo, y me gustaría contar con vuestra colaboración tanto en los proyectos que ya tenemos en marcha como en los nuevos que se iniciarán. En estos meses hemos aplicado el principio de la homeostasia que gobierna la fisiología a nuestras vidas: hemos aprendido que podemos cambiar nuestra forma de vivir y trabajar para adaptarnos al nuevo medio que nos rodea. Son muchos los proyectos e ilusiones que han quedado en el camino, pero debemos seguir luchando y recuperar las fuerzas, el entusiasmo y la motivación para no dejarlos abandonados, y así lo hemos hecho en la Asamblea General celebrada el pasado 26 de octubre, en modalidad virtual. En dicha Asamblea se decidió que el 40 Congreso de la SECF mantenga su celebración en Badajoz en el año 2022, algo que merecía el Comité Organizador por el gran trabajo realizado desde su elección como sede en el Congreso de Cádiz en 2018. Se informó de la aceptación por unanimidad de los miembros de la FEPS de la candidatura de Granada para celebrar su próximo congreso en septiembre de 2021, en modalidad presencial, siempre que la situación lo permita. Los profesores Dr. D. Vicente Notario y Dra. Dña. Ana Ilundaín, dos grandes fisiólogos y premios “Juan Negrín” y “Antonio Gallego” respectivamente, nos dedicaron unas emotivas palabras como anticipo a la entrega presencial que se realizará en la sesión que la SECF celebrará en el próximo Congreso de la FEPS. También nos dedicaron unas palabras de agradecimiento las premiadas por la Sociedad a la “Mejor Tesis Doctoral” (Dña. Eliana Barriocanal Casado) y “Premio SECF de Divulgación Científica” (Dña. Belén Gago Calderón).

En estos momentos en los que la comunicación ha cambiado a un entorno on-line se hace más importante que nunca el empleo y uso de nuestra página web (h�ps://www.secf.es) en la que encontrareis toda la información actualizada sobre las actividades y marcha de la sociedad. Os animo a tomar parte activa en esta comunicación haciéndonos llegar vídeos resumen de vuestra actividad investigadora y docente; a que participéis en nuestra revista científica, a cuyo Comité Editorial agradezco el enorme esfuerzo que realiza; y a que nos enviéis vuestras sugerencias de mejora e innovación; os animo además a seguir a la SECF en redes sociales (Facebook, Twi�er e Instagram); en definitiva, os animo a que os impliquéis con nosotros ya que os necesitamos para poder avanzar como Sociedad.

Agradezco a la anterior Junta Directiva la gran labor realizada y su desinteresado trabajo, especialmente a los que, tras seis años de intensa actividad, acaban su periodo en ella. Todos los miembros de la actual Junta os deseamos que, a pesar de la pandemia que vivimos, podáis disfrutar de unas muy felices fiestas llenas de salud y amor que, aunque sea en la distancia, siempre se puede transmitir. Que el próximo 2021 nos traiga el retorno a la ansiada normalidad que todos deseamos, pues hoy por hoy es nuestra felicidad. Muchas gracias a todos por formar parte de esta Sociedad.

Un abrazo

Meritxell López Gallardo

Presidenta Ejecutiva de la SECF • INSTRUCCIONES A LOS AUTORES A. Remisión de originales La remisión de originales se hará exclusivamente por correo electrónico a la dirección del editor o de cualquiera de los miembros del comité editorial. Se puede utilizar cualquier procesador de texto, programa y formato gráfico, aunque es preferible remitir el manuscrito en formatos usuales. En todo caso deben indicarse en la carta de remisión los formatos empleados para texto, tablas, gráficos y fotografías. La utilización de formatos poco usuales retrasará la publicación. En caso de emplear algún sistema de compresión para fotografías o gráficos, debe comprobarse que la descompresión no deteriora la calidad de las imágenes. La carta de remisión debe incluirse en el cuerpo del mensaje electrónico y el original y las figuras en forma de archivos anexos. El texto del artículo debe adjuntarse como un único archivo, incluyendo la página con el título, el texto principal, bibliografía, etc. Cada tabla o figura debe remitirse en un anexo independiente, nombrando cada anexo con el nombre del primer autor y el número de tabla o figura que contenga (ejemplo: Cunqueiro-Fig.1). Direcciones comité editorial: Juan Antonio Rosado ([email protected]), Diego Álvarez (Universidad de La Laguna, [email protected]), Teresa Giráldez (Universidad de La Laguna, [email protected]), Celestino González (Universidad de Oviedo, [email protected]), Ana Ilundain (Universidad de Sevilla, [email protected]), Juan Martínez-Pinna (Universidad de Alicante, [email protected]) y Carlos Villalobos (CSIC, [email protected]). B. Composición de los originales 1. Primera página. •Título •Autores •Filiación de los autores •Autor y dirección para correspondencia si procede (incluir números de teléfono y fax, y una dirección de correo electrónico). 2. Segunda página. Sumario, si procede, en una extensión un superior a 200 palabras, en el mismo idioma que el resto del artículo. 3. Cuerpo del texto. Los artículos no deberán sobrepasar las 2.500 palabras e irán en folios numerados. Deberán estar escritos en un estilo claro y con pretensión divulgativa, de forma que puedan ser entendidos por cualquier fisiólogo, independientemente de su área de especialización. El procedimiento más simple es tomar como ejemplo cualquier artículo publicado previamente en Fisiología. En caso de no disponer de ningún ejemplar, puede solicitarse a cualquiera de los miembros del comité editorial o a la Secretaría ([email protected]) para ser incluido en la lista de distribución. Alternativamente, pueden consultarse los artículos de los números anteriores en http://www.seccff.org Los artículos podrán contener resultados ya publicados, siendo entonces responsabilidad exclusiva de los autores obtener los permisos correspondientes de las revistas o libros donde hayan sido publicados originalmente. Debido a la pretensión divulgativa, cada autor podrá organizar el texto en la forma que crea más oportuna, si bien se sugiere una división en secciones que facilite su lectura. 4. Otros. a.Notas (si las hubiere) y agradecimientos. b.Bibliografía. Las referencias, muy seleccionadas, se insertarán en el cuerpo del texto entre paréntesis (ejemplo: Chacón y Mairena, 1999). La relación completa de referencias bibliográficas deberá incluirse al final del texto, por orden alfabético y cronológico, de acuerdo a los formatos más habituales. Ejemplo: Gómez J, Belmonte J (1910) Deciphering bullfighting. J Taurom 57: 200-235. c.Pies de figuras. Deberán incluirse a continuación de la bibliografía y en páginas aparte. d. Figuras. Su número no deberá ser superior a 2-3 por artículo, y el tamaño máximo aceptado será el de una hoja impresa (DIN-A4). En el caso de figuras previamente publicadas, si fuere necesario, deberá acompañarse autorización para su reproducción en Fisiología. e.Tablas. 1C). calleddiverse somatosensation is what stimuli in of sensing (Figure the upon divalent) flow and mono- (mostly segments S5-S6 cations where pore the where define the basic subfamilies. The transmembrane S1-S6 TRP the definedsubunit by is domain, of diversity the defines correspondingand functional structural properties and andS6.(Figure1B).ThediversityofN-andC-terdomains S5 pore-forming transmembrane between loop (S1-S6) a six-segment with (TMD), domain a and terminal C-superfamily cytosolic and two domains consist N- of repertoireTRP al.,2011). (Saito et terrestrial and sequence divergencefollowed current by constitute the fishes teleost vertebrates through of that repeated duplications gene the ancestor and from common came superfamily diversity TRP 2013). al., classified are functional (Clapham 2003; role Perálvarez-Marín al., which et their 1A), by et not sequence (Figure their homologyregarding and TRPML channels to TRP (vanilloid), 27 TRPV (mucolipin) (polycystic). (melastatin), TRPP are humans and there In TRPM TRP (canonical), (ankyrin), TRPC Mammalian on members; founding subfamilies based 1969). six into divided Manning, superfamily is and firstly(Cosens were channels Drosophila mutant strain of described These a melanogaster in 2013). (Zheng, stimuli physical in chemical and spectrum of wide act as a response to to act capable being that sensors, channels cellular polymodal cation non-selective of group superfamilyTRP Tel: 1907 de 581 Facultat 93 +34 Molecular, Fax: 1907 Biologia Spain 581 de Catalonia, Vallés, i 93 del +34 Cerdanyola Bioquímica 08193 de Barcelona, Departament de Autònoma Biofísica, Universitat Medicina, de Unitat encBiofísica, d’Estudis Perálvarez-Marín. A. Centre and Enrich-Bengoa J. correspondencia: la para *Autor ² Spain Bellaterra, 1 Jennifer Enrich-Bengoa PATHOPHYSIOLOGY. SYSTEM NERVOUS CENTRAL IN PLAYER ELUSIVE AN TRPV2: nttd ifsc,Dpraetd iqíiaid ilgaMlclr nvria uòoad acln,013 08193 Barcelona, de Autònoma Universitat Molecular, Biologia de i Bioquímica de Departament Biofísica, de Unitat nttt fNuocecs nvria uòoad acln,013Blaer,Spain Bellaterra, 08193 Barcelona, de Autònoma Universitat Neurosciences, of Institute hscto hne ntecneto ua hsooy optteftr ou nterl fTP2i eta central in TRPV2 of role the on focus future the put to physiology, human pathologies overview of to pathophysiology. to context aim system we nervous the associated TRPV2, in regarding being revision channel metabolism, this cation In and cardiomyopathies. this and immunity, cancer plays dystrophy, function, TRPV2 muscular tissues. neuromuscular as human such in cardiac, expressed in ubiquitously Among is roles pathophysiology. TRPV1, of in distinct homologue targets closest pharmacological the important TRPV2, channels, are TRP channels (TRP) Potential Receptor Transient ttesrcua ee l ebr fTP TRP of members all level structural the At Transient receptor a potential channels are (TRP) 1,2 n lxPerálvarez-Marín Alex and 1,2 . RVsubfamilyTRPV l,21) speiul ad RV- hnesae are channels TRPV1-4 said, previously As 2013). al., subfamily, (Perálvarez-Marín this TRPV1 of member et characterized most homology the the to VRL-1 based on as firstly named was mammalian subfamily TRPV and TRPV2 physiology pathophysiology and homeostasis activated not are and heat (Montell, by Ca 2005). general calcium-selective for important channels osmolality.and other TRPV5-6 group formed The by are spectrum functions of wide nociception, such as a involved being in described thermoception been for has group considered thermosensitive activated are heat. This as by spectrum physical wide chemical of and stimuli,a being permeablelow calcium activated channels be can and by 2002). non-selective mainly TRPV1-4 formed group by is TRPV2 sequence show (Gunthorpe identity 50% al., of et Ca for selective TRPV5-6 respectively, 75%, and TRPV1-4 being non-selective and globalTRPV5-6 sequence groups, a identity 20% with of their sequence homology cation to a�ending selectivity; this and groups two TRPV1-4 of and members into divided six are family The types. cell and tissues body practically all distributed widely in are subfamily that olfactation, osm-9/ four mammals, members six there are (TRPV1-6) TRPV the in in other receptor related and 2011). In (OCR-1-4) genes Xu, and (Xiao involved OSM-9 channels; TRPVs is 5 total elegans of al., 2013). C. a Marín there et In is OSM-9 mechanosensation olfactory and adaptation (Perálvarez- family 1997). abnormal avoidance Caenorhabditis from al., (osmotic elegans 9) (Colbertmember et OSM-9 was h is eotdmme fteTP subfamily first reported TRPV The the member of RV stems nnw ebro h the of member unknown most the is TRPV2 2+ epciey RV n and respectively. TRPV1 , 2+ - 4 -

FISIOLOGÍA. Boletín informativo de la SECF hwn h i-rnmmrn emns n h yooi -adC emn.I akbu,tesget 5S, S5-S6, segments the blue, dark In termini. C- and N- cytosolic the and segments, six-transmembrane the showing sativa derivatives potent are agonists TRPV2, of specie-dependent. also are demonstrated been has It that these compoundssome of specific not are TRPV2 for and pharmacology knowledge limited, still the and in but is knownis that TRPV2 activated is noxious at temperatures thermal responses wild-type 2011). al., It to (Park et mice elusive this of channel activation endogenous (Fricke al.,2019). et of report first specific of Oxidation methionines stress. drive TRPV2 cation influx, in becoming oxidative the by activated endogenouslyRecently, shown been TRPV2 that is has it temperature in TRPV2 sensing remainsof controversial. 2013). al., Perálvarez-Marín activationTRPV2 temperature et 1999; is role dependent the but al., et chemical compounds(Caterina some modulated by be also can and °C) activated noxious (>52 heat is TRPV2 by of case the In (Tominaga, different stimuli 2007). activated by are them temperature of threshold activation of all different and a have one each temperature dependent and urudn h o hne ae C hsooia vriwo h R-eae aintasotpoesi h the S1-S4, in segments process transmembrane transport the cation orange TRP-related In the pore. of ion overview the Physiological (C) forming process. physiological gate. and somatosensation channel channel ion the the of surrounding center the in clustered iue1 R uefml eetie repertoire. superfamily TRP 1. Figure tde naTP2koku ieso similar show knockout mice TRPV2 a Studies in A ua R ufmle hlgn.()TPsrcua etrs features, structural TRP (B) phylogeny. subfamilies TRP Human (A) irl(ui ta. 07 eávrzMrne l,2013; Perálvarez-Marín al., 2007; et al., et (Juvin citral SKF96365, TRPV2; compound,diuretic for specific amiloride, Ruthenium not trivalent Red, related are cations and identified they although been have blockers TRPV2 A Some 2007). al., 2007). mouseTRPV2but human(Chung not al., al.,2005;Juvinet et activate to able diphenylboronic et is 2007; anhydride (DPBA) al., et Juvin Neeper 2004; al., human et being insensitive (Hu species, TRPV2 among variable is the sensitivity agonist and TRPV2 TRPV2 for specific first not the identified, is however was compound This APB). TRPV2 modulation 2-Aminoethoxydiphenyl is effects shown on compound 2009). Other has al., that borateet (2- least activators TRPV2 of Petrocellis (De al., 2011; et Vriens stronger Cannabinoic activators the TRPV2. are acids of delta-9-tetrahydrocannabivarincannabidiol and the are sativa derivatives, (−)trans-delta-9-, 2008). cannabis Among al., et Qin Petrocellis 2011; al., et De 2013; to al., (Perálvarez-Marín physiology compounds TRPV2 of et these effect the to assess difficulties the leading to TRPV2 specific for not are although they - 5 -

FISIOLOGÍA. Boletín informativo de la SECF ,-ilbs1ehlunlnu)didd Lmn(K4) N-(Furan-2-ylmethyl)-3-((4-(N7-methyl-N′- (NK-4)); (Lumin diiodide and agonists 4,4′-[3-[2-[1-Ethyl-4(1H)-quinolinylidene]ethylidene]-1-propene- TRPV2 TRPV2: for (B) code 1,3-diyl]bis(1-ethylquinolinium) antagonists PDB (LPC). brain. form TRPV2 Lysophosphatidylcholine derived the (2-APB); for structure diphenylborinate Abbreviations in 2-Aminoethyl TRPV2 agonists: pharmacology. stimuli TRPV2 and for physiology physicochemical Abbreviations CNS 6U88. several in impact for potential with sensor antagonists environmental an becoming (Hisanaga 2009) al., suggest et TRPV2 involvement the in expressed in pancreatic also studies β-cells performed Kojima Lab and is by circulatory TRPV2 system. the in al., 2010). et (Peng These rats evidences in veins suggest possible the of cells muscle smooth TRPV2 role of in and rabbit al., 2003) human (Park and (Fantozzi et and al., 2003), et both; (Iwata arteries endothelial in localized in of and muscle smooth cells been also has TRPV2 patients Matsumura, 2019). for DMD target therapy possible a in cardiomyopathies as studied being also this is to contributing myocites pathophysiological dystrophic phenotype in 2015). al., (Lorin TPRV2 et influx defective been Ca a in has contribution TRPV2 as observed the of such pathologies it muscular (DMD), dystrophy some muscular Duchenne In 2014). al., et cardiac functionand (Katanosaka Rubinstein 2014; al., et necessaryTRPV2 correct is a maintenance for structure of observed been has 2009; Watanabeal., that 2009). al., It et al., 2017; al., 2015; Lorin Robbins et al., 2013; Sabourin et et skeletal cardiac and muscle (Ague�az al., 2017; Jones et et 2011). recent In years, al., phenotype(Park gaining TRPV2 is TRPV2 much mild a�ention et in a present thus knock-out mice 2019a), al., impairment different could to lead pathologies, et (Doñate-Macián although body TRPV2 for affinity higher show them (Perálvarez-Marín of al.,2013). et both but inhibitor, specific and TRPV2 activator respectively. not compounds are These as tranilast, and specific 2009). More al., modulators TRPV2 Vriens et are rplmn)6(rfurmty)prmdn2y)ho-rpnmd ST) rcioolehnlmd AA; (AEA); ethanolamide (LEA). ethanolamide linoleoyl arachidonoyl (SET2); propylamino)-6-(trifluoromethyl)-pyrimidin-2-yl)thio)-propanamide iue2 ATP2cosaki N. CNS. in crosstalk (A)TRPV2 2. Figure RV suiutul xrse hog h the through ubiquitously expressed is TRPV2 RV sepesdi irgi,atoye,adnuosi N, CNS, in neurons and astrocytes, microglia, in expressed is TRPV2 2+ CSadPS respectively) fine-tuning PNS, charge of and of (CNS in expressed central both peripheral and in nervous system nervoussystem.It isalready known that TRPV2iswidely proliferation questionthe physiological about the and the TRPV2 in survival of role importantly more se�les cell 2013), 2010, but al., (Nabissi , et glioma of regulator conclusion the to lead TRPV2 that negative functions a as chemotherapeuticeffects the of human cytotoxic agents. observations This the chemosensitivity of to Glioblastoma cells the multiforme increasing (GBM) by lines glioma cell human apoptosis induces the expression by of increasing TRPV2 that 2008; suggest studies al., et (Caprodossi lines 2020). Recent al., Doñate-Macián 2018a; Santoni et al., cell et and types cancer tumor overexpression TRPV2 several and in 2014). found been has oncogenic al., with carcinogenesis during suppressor (Liberati associated et roles been down-regulationhave and up TRPV2 years. last the during TheroleofTRPV2incancerhasalsobeenafocusofstudy 2013). al., Perálvarez-Marín Santoni et 2014; 2013; al., et Nagasawa,regulating (Kojima system immune and the different cells immune in spleen, also types of and organs as in such found is channel This 2013). al., et Santoni 2010; al., et Link 1999; al., (Caterina system et immune the relevant in also expressioninsulin action. TRPV2 is otadtieia agi Alwlae l,2002; al., Caterina et (Ahluwalia al.,1999; Ichikawa et ganglia Sugimoto, as trigeminal and 2000). and root channels dorsal especially in (PNS), system peripheral nervous TRP in studied widely somatosensory been receptors have signaling. cation-mediated - 6 -

FISIOLOGÍA. Boletín informativo de la SECF motn RV neatr uha B,FF, FGF1, ABR, as KCNJ10, PEBP1, such PLP1, SDC3 proteins. and interactors TRPV2 important article identified this as been neoplasm also and have in diseases CNS proteins involved in Other 2018a). al., et (PLP1), Opalin, neurotrimin and (NTM) (Doñate-Macián proteolipidmyelin proteins CNS, such as the protein in 1 protein- be�er protein on interactions. based channel to this found cohort, the Some interactors of TRPV2 of patient role key are understand the the GBM discover using by to interactors approach proteomics and two of these mechanosensory trafficking constitutive cation channels. and regulated the proteins laboratory, involved the in our about from Perálvarez- Doñate-Macián and 2019b) 2019a, 2018b, Doñate-Macián al., 2014; 2015; Marín, et al., et Macian published other results with points out, trafficking. papers (Doñate- These in interactors involved TRPV4 and (Doñate-Macián CNS lab TRPV2 2018a) show our al., from et in (re)myelination. obtained TRPV2 Results in of role development an the perspectives in new add laboratoryresults our from These (Doñate-Macián 2019). Amantini, the 2018a) al., and et (Santoni of system diseases nervous and neoplasms other in involved with proteins and proteins myelin key laboratoryinteracting is with TRPV2 our that revealed 2018a) in al., results (Doñate-Macián published et recent also and physiologyCNS (Cohen al., 2015; Shibasaki et al., 2010) et and osmoregulation balance (Perálvarez-Marín al.,2013). to et osmosensory osmotic maintenance mechanisms and of in channel related this somatosensation, of role suggesting the brain structures localization correlates with TRPV2 2008). al., et expressing highest the mouse forebrain neurons the of regions in TRPV is (Cahoy TRPV2 2008). al., et (Cahoy (Wainwright al., 2004) mature the et and forebrain mice in macaques hypothalamo-neurohypophysial the 2012), in al., (Nedungadi system et forebrain and rats the in hindbrain regions and 2005) Wood, been and (Liapi also cortex has channel This cerebral importantdetected the in regions, brain oxide. as such nitric and microglia,stress In 2019). al., oxidative phagocytosis upregulated and by are TRPV2 et (Maksoud microglia and astroglia other glial as cells such (Shibasakiin 2013) al., et al., 2015; Shibasakiet al., 2010). et also expressed TRPV2 is neurite outgrowth and sensory motor and axon of neurons the needed (Cohen for also and 1999) al., (Caterina et medium-to-largein myelinated neurons have that fibers interesting regulatory specifically target. TRPV2 is found becoming (Figure types 2A) an severalexpressed cell in central the TRPV2 in nervous system eetsuisb an ta.(an ta. 2016, al., et (Hainz al. et Hainz studiesRecent by laboratory our performed been In silico has in it an the in role already TRPV2 plays a known that is It is (CNS) system nervous central in TRPV2 rmsn oeta o h td fTRPV2 (Figure myelination 2A) in during development CNS of and TRPV2-mediatedthe types cellular study cell crosstalk CNS of research develop regarding line a to idea a�racted the the to with for pathophysiology. 2B), potential these evidences, With all have been (Figure we identified and promising agonists being TRPV2 specific are antagonists and new but elusive, 2005). pharmacological the At in al., (Pla�en level, et experimental TRPV2 remained has this TRPV2 model outcome in MS of importance blocker TRPV2) for ameliorates the mice paralysis improving suggest myelination. study using tranilast EAE mice specific A also (a and TRPV2 seems another important point interest of study to activating TRPV2, simultaneously. Effects Panx1 and inhibiting pathway on dual by Panx1 and a exert may EAE probenecidHowever, working hypothesis that our in oligodendrocytes is responsible death. of is that (Panx1) channel pannexin-1 ion probenecid demyelination/remyelination the ATP effects of in inhibitory the on focus al. et Hainz the of 2017b). al., (Hainz et demyelination in model reduce and curprizone 2017a), 2016, al., autoimmune encephalomyelitis (Hainz et mice in (EAE) progression experimentalthe clinical an symptoms of in specific prevent arrest agonists, TRPV2 capable and to is most the probenecid, of 2017a, 2017b) showed how one noxious heat. Nature 398,436–441. threshold for high capsaicin-receptor a A (1999). homologue with Julius, D. and Caterina, Brake, Tominaga, A.J., T.A., Rosen, M.J., M., 612–620. bladder: of 54, pathologichuman correlation carcinoma urothelial Urol. the Eur. stage. with in and urothelium normal in expression (2008). 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GDM miR-17-5p, plasma of samples in miR-16-5p, miR-20a-5p and of miR-19b-3p miR-19a-3p, upregulation the study pilot their in reported authors the These 2015). al., although et (Zhu women, miRNAs healthy of set different a vs. involved observed changes GDM in gestational weeks at 16-19 of c-miRNAs profile differential a described been also has Additionally, it 2018). (Pheiffer al., weeks et gestational 13-31 at women GDM of serum the in lower also was miR-222 expression of the that observed study recent more a instance, For NAs. miR- certain of expression the with GDM of sociation as- the describing group published been has information GDM amount considerable of a then, the Since 2011). al., in et (Zhao decreased significantly were miR-222 and miR-29a-3p, miR-132, 2011). of expression al., The et (Zhao chips (TLDA) Array Density Low Taqman the using by screening systematic a on sisted con- weeks) gestational (16-19 pregnancy early tively h is td osdrn eu -iNsa as c-miRNAs considering serum study first The profiles c-miRNA analyzed have authors Most 3- 13 -

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Boletín informativo de la SECF esai n usqetyicesdtelvlo of level the increased subsequently and meostasis ho- glucose regulates that protein membrane re- ticulum endoplasmic an level, expression Insig1 increase could miR-29a of trimester of downregulation the Thus, pregnancy. expression on depending an changes presents that pa�ern miR-29a Finally, 2018). et (Pheiffer al., GDM in resistance insulin estro-gen-induced in expression regu- (ERa) potential a receptor a estrogen of is lator it and cells stromal endometrial proliferation of with associated miRNA placental a This weeks. gestational is 13-31 at women GDM in descri-bed been has miR-222-3p of downregulation The 2012). al., hypoxia-res- et (Wang many VEGFA including genes, of ponsive expression the regulating gh throu- function development placental and for critical tension oxygen to sensitive highly transcription a factor is HIF1A IL-8. and TIMP2, they VEGFA, MMP2, HIF1A, because pregnancy, as such abnormal process this for important genes an several target to lead ght mi- miRNAs these of upregulation and angiogenesis with associated are miR-20a-5p and miR-17-5p their part, For 2011). al., et (Kantharidis resistance insulin causing signaling, insulin block will women GDM miR-16-5p in of upregulation the thus, 2, (IRS) and substrate 1 receptor proteins insulin the encoding targets miR-16 genes example, For 2015). al., sig- et mTOR (Zhu naling and signaling, TGF-β mellitus, diabetes 2 type signaling, insulin diag- signaling, MAPK pathways: GDM and five associated with mainly tested are miRNAs These nosed. is weeks) (24-28 normality ab- glucose serum before is, that pregnancy, of weeks 24–28 and weeks 20–24 weeks, 16–20 at women GDM of plasma in upregulated are miR-17-5p which miR-20a-5p, miR-16-5p, and consider could the we On hand, blood. one maternal from obtained when c- GDM, of biomarkers which promising most about the drawn be could be miRNAs can conclusions some 1), different the studies. in observed results heterogeneous the in resulting strategies, normalization and analysed, miRNAs of number and type measurement platform, characteristics, population by analysed, biological sample gestationalincluding age, affected be may expres-sion miRNA Furthermore, each. study descri- one been in only bed have they expression although altered GDM, an during 2019, exhibit miRNAs to al., other reported et been Many have Hocaoglu 2019). 2018, al., al., et Martinez-Ibarra et Stru� 2018, al., stu- the Houshmand-Oeregaard 2017, of al., et (Sebastiani et rest dies the for comparable hardly and neous 2013). al., et deve- (Collares in GDM the of lopment miRNAs specific the of one as identified l,cuighprlcma(hoe l,2011). al., et hyperglycemia (Zhao causing lls, ce- hepatic gluconeogenesis in in enzyme key a PCK2, ept h eeoeet ftersls(iue (Figure results the heterogeneity of the Despite heteroge- complex, more even is scenario The iN rfl hogottetretietr f deve- of who those trimesters in and women three healthy in pregnancy the no throughout know, profile we miRNA c- the as in changes far the analysed has As study longitudinal biomarkers. as value as well their as gestations, th- diabetic c-miRNAs and healthy of roughout role regulatory the on perspective translational of terms in value. diagnostic results and the of impact the ve tremendously impro- would that priority a be should analysis data miRNA for strategy common and solid a common of existence The a GDM. define to or criterion diagnostic processing data for procedure ac- globally cepted and solid a of lack the as limitations, such several also are There methodological approaches. experimental the and in differences huge most to due comparable, likely hardly and heterogeneous of quite biomarker are a reliable studies different the in obtained results The GDM. provide profile specific a c-miRNA nor c-miRNA single at a neither GDM, moment during this occur profile miRNA plasma the in perspectives Future hmSS hn ,Hn ,LugTY a ,Ci , mi- 482-490. 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J Sanz-Esporrin J, Gonzalez-Febles Bascones-Martinez A, References risk. metabolic reduce to aimed interventions lifestyle of implementation and design the optimizing inheritance, risk transgeneratio- metabolic the nal of understanding be�er a in help preg- also would during information This syndrome GDM. obstetrical including nancy, of kind any lop utemr,teei tl ako aaon paramount a of lack a still is Furthermore, there changes that accumulates evidence Although 4- 14 -

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FISIOLOGÍA. Boletín informativo de la SECF nelui-7i ettoa ibtsmliu.JCl hso 3:7141- 234: Physiol 7148. Cell J mellitus. diabetes gestational in interleukin-37 targeting via response Dysregu- inflammatory (2019). influences microRNA-657 Z Wang of P, Teng lation X, Xiu X, Zhang C, Li H, Wang P, Wang circulation and heart in 433-441. MicroRNAs 7: (2018). Sci Health Sport J J exercise. physical Xiao during G, Li Y, Lv L, Wang 431-441. 66: J Endocr mellitus. diabetes gestational with women of of placentas profile Expression (2019). in B RNAs Yu circular J, Miao K, Liu W, Zhou G, She H, Wang Clin Res Diabetes diabetes. 1-9. 132: gestational Pract of risk and microRNAs nancy mid-preg- and early- Circulating (2017). K, A T D Sorensen Enquobahrie G, A, M Tadesse M Williams J, V Parikh K, Hevner J, E Boyko L, P Wander 4-27. 8: their Microrna Databases. Biogenesis, and Web-based Tools, Biology, MiRNAs: (2019). E Hasheminasab M, Tafrihi elts n yaclOse 3:49-53. 130: Obstet Gynaecol J Int mellitus. diabetes gestational predict plasma to maternal Profiling pregnancy (2015). early Q in Ge expression microRNA J, Lu Y, Zhou H, Li F, Tian Y, Zhu 960. 953- 46: Biochem pregnancy-specific Clin diseases. for biomarkers as NAs miR- for potential Diagnostic (2013). M A Gronowski H, K Moley Z, Zhao miRNA serum second-trimester Early J, e23925. (2011). Dai 6: R, One J PLoS mellitus. Huo diabetes gestational Sha predicts profiling J, Z, Xu D, Hu Chen S, Y, Pan Zhu B, Y, Yu Xia Z, Shi T, Jiang J, Dong C, Zhao E1051-1059. 97: Metab Endocrinol Clin J placenta. human and ephrin-B2 in EPHB4 target that -20b) and -20a, miR-17, (i.e., microRNA ciated angiogenesis-asso- up-regulates Preeclampsia M, (2012). Parast B C, D L Laurent Chen S, J, Satohisa Zheng S, Hachy H, Zhang L, Feng W, Wang 6- 16 -

FISIOLOGÍA. Boletín informativo de la SECF .Sensibilidad somatovisceral8. Murcia) (Univ. Pérez Madrid Antonio Juan Receptores sensoriales. sensitivas7. Vías Coordinador: Sacristán García Albino NERVIOSO SISTEMA II: PARTE Sacristán Complutense García (Univ. Albino Madrid) Transmisión sináptica. neuromuscular6. Unión Complutense (Univ. Arcos Madrid) los de Rivera Luis liso músculos cardíaco y los Contracción de 5. Complutense (Univ. Arcos Madrid) los de Rivera Luis esquelético músculo Contracción del 4. Benedito Castellote ComplutenseSara (Univ. Madrid) nervio Fisiología del 3. Coordinador: Sacristán García Albino MÚSCULO NERVIO Y FISIOLOGÍA DEL PARTE I: Extremadura) (Univ. Ruiz Salido M. Ginés Comunicación vital celular.2. Ciclo Sacristán Complutense García (Univ. Albino Madrid) Evolución. Concepto. Homeostasis Fisiología. la a Introducción 1. h�ps://www.tebarflores.com/inicio/285-fisiologia-veterinaria-9788473606448.html 978-84-7360-571-7 ISBN: páginas 1296 mm 280 x 200 (editor). Sacristán García Albino VETERINARIA FISIOLOGÍA .Ftreecó,e j avsó visión la y Fotorrecepción, ojo 9. el Murcia) (Univ. Pérez Madrid Antonio Juan acaScitn ue aetveaa rned tocncd aulqedrneao asd eeecae l el en referencia sido Albino ha de años general durante edición que la manual conocido con otro contado de materia, ha frente cada que al en sector. manual, estuviera especialidad completo ya su este quien por desarrollar Sacristán, seleccionados García de internacionales, encargados 6 los y sido al españolas han universidades exclusivamente 9 orientado de didáctico, autores y 58 los atractivo comprender a esquemático, autores: estudiante modo esta Los al a un ayudan acuerdo de de que actualizado texto animal. color y mundo a el ampliado ilustraciones en han de se explicados cientos obra conceptos incluido la componen han que se cada de de temas Además, lugar constante 82 evolución. revisión en los la biofísicos, y motiva ello, que Por lo moleculares funcional. independientes, vivos. términos proceso biológicos seres fenómenos en los de de más, serie fisiológicos vez una procesos como cada los simplemente a explicarse, 82 respuestas pueden nuevas primera y logrado fisiológicos por han coordinara mecanismos temáticos se Sacristán Los libro, García bloques este Albino de Fisiología 11 edición de primera catedrático en la el vez que divididas públicas desde internacional. Veterinaria transcurridos páginas, de ámbito años Un facultades de 20 1300 las veterinaria. los universidades todas En 6 casi la casi otras de de de como catedráticos así profesionales y largo España, profesores para intervenido de lo han indispensable que a texto el que en extiende autores un y los capítulos, se manual de prestigio este que y de calidad proyecto la hacen como ambicioso ella, así obra, en la intervenido compendia que han contenidos de amplitud y dimensión La libro: el Sobre IRSRECOMENDADOS LIBROS 9 ecctsogóuo lno blancos glóbulos o Leucocitos 19. Madrid) Complutense (Univ. Visedo Recio Paz hematíes o rojos Eritrocitos, glóbulos 18. León) (Univ. Lera Barrio Pablo Juan corporales Fluidos 17. Coordinador: González Gallego Javier INTERNO MEDIO III: PARTE Murcia) (Univ. López Salvador Ruiz vigilia. Conducta animal y Sueño 16. Sacristán Complutense García (Univ. Albino Madrid) nervioso Sistema autónomo 15. Córdoba) (Univ. Carmona Agüera Sergio funciones superiores las cortical Control de 14. Córdoba) (Univ. Carmona Agüera Sergio cerebelo Ganglios y basales 13. del Córdoba) (Univ. y Carmona Agüera Sergio espinal médula la encéfalo del tronco de motoras Funciones 12. Extremadura) Dionisio (Univ. Rosado Antonio Juan Quimiorrecepción11. Extremadura) Pariente Antonio (Univ. Llanos José audición la Fisiología de 10. Rodríguez Moratinos Extremadura) (Univ. B. Ana 7- 17 -

FISIOLOGÍA. Boletín informativo de la SECF ead .HrádzRdíuz(C) (UCM) Rodríguez Hernández V. Medardo urinarias vías las de Fisiología 39. León) (Univ. Gutiérrez Mauriz Luis José ácido-base Equilibrio 38. León) (Univ. Peláez Merino la Gracia de dilución y orina concentración de Mecanismos 37. León) (Univ. Felipe de Álvarez Isabel Ana tubular Función 36. León) (Univ. González Tuñón Jesús María renal Función 35. Gallego González Coordinador: Javier EXCRETOR SISTEMA VI: PARTE Zaragoza) (Univ. (†) Herrero Alcalde Isabel Ana aves las en respiración la de Fisiología 34. Zaragoza) (Univ. Silanes de López Murillo Divina Mª respiración la de Regulación 33. Alvarado, Venezuela) Lisandro (Univ. Cortez Matheus sangre Nyurky la de través de a gases de Transporte Autónoma 32. (Univ. Farrerons Barcelona) Jiménez membrana la Marcel de través a respiratoria gases de Intercambio 31. Zaragoza) (Univ. Silanes de López Murillo Divina Mª Ventilación pulmonar 30. Silanes de López Murillo Divina Coordinadora: Mª RESPIRATORIO SISTEMA V: PARTE Córdoba) (Univ. Durán Escribano Mª Begoña especiales áreas por Circulación 29. Madrid) Complutense (Univ. Ocejo Prieto Dolores vascular circulación la de Regulación 28. Córdoba) (Univ. Durán Escribano Mª Begoña capilar y venoso arterial, Pulso sanguínea Presión 27. Córdoba) Valenzuela Santisteban (Univ. Rafael sanguíneos vasos los de Fisiología 26. Argentina) Plata, El la de Nac. (Univ. Trigo I. Pablo cardíaca actividad la de corazón. Regulación 25. Córdoba) (Univ. Buendía Agüera Estrella cardíaco del ciclo El 24. Córdoba) Valenzuela Santisteban (Univ. Rafael Electrofisiología electrocardiograma 23. Córdoba) (Univ. Luque Rubio Dolores María circulación la Consideraciones sobre generales 22. Montijano Castejón Coordinador: Francisco CARDIOVASCULAR SISTEMA IV: PARTE León) (Univ. Campos Sánchez Sonia Hemostasia 21. León) (Univ. Collado Sánchez Pilar inmunidad e Linfocitos 20. León) (Univ. Galiana Almar Mar oriao:GnsM aioRi Ruiz Salido M. Coordinador: Ginés DIGESTIVO SISTEMA VII: PARTE oriao:Li eied aCu aoio Palomino Cruz la de Felipe Coordinador: Luis ENDOCRINO SISTEMA VIII: PARTE Rodríguez-Yoldi Zaragoza) Jesús (Univ. María intestinal absorción de Procesos 50. Extremadura) (Univ. Liberal Redondo Cosme Pedro aves las de digestiva Fisiología 49. Zaragoza) (Univ. Loshuertos Arruebo Pilar Mª rumiantes los de digestiva Fisiología 48. León) (Univ. Gallego González Javier biliar secreción y Hígado 47. Extremadura) (Univ. Dionisio Rosado Antonio Juan intestinal Secreción 46. Extremadura) (Univ. Almaraz Camello J. Pedro exocrina pancreática Secreción 45. Extremadura) (Univ. Almaraz Camello Cristina gástrica Secreción 44. Extremadura) (Univ. Mateos González Antonio salival Secreción 43. Zaragoza) (Univ. Carrión Plaza Ángel Miguel digestivo tracto el en alimentos los de Transporte 42. Extremadura) (Univ. Mateos González Antonio Ingesta 41. Extremadura) (Univ. Pascual y Pascual Rosario Mª Nutrición 40. srlaAür uni Ui.Croa Córdoba) (Univ. Buendia Agüera Estrella masculino genital Aparato 64. Palomino Cruz la de Felipe Coordinador: Luis REPRODUCTOR SISTEMA IX: PARTE Santiago) (Univ. Diéguez Carlos crecimiento del Fisiología 63. Portugal) Douro. Alto Trás-os-Montes e (Univ. Oliveira de Martins A. Paula Prostaglandinas Timo. Riñón. 62. Madrid) Complutense (Univ. Visedo Recio Paz adrenal Médula 61. Alto Portugal) Douro. e Trás-os-Montes (Univ. Colaço Antunes Aura adrenal Corteza 60. Coruña) A (Univ. Carballido Cordido Fernando páncreas del endocrinas Secreciones 59. Extremadura) (Univ. García Tapia Antonio José gastrointestinales Hormonas 58. Santiago) (Univ. Vieytes Rodríguez Mercedes fósforo y calcio del reguladoras Hormonas 57. Santiago) (Univ. Palomino Cruz la de Felipe Luis Tiroides 56. Santiago) (Univ. Vieytes Rodríguez Mercedes pineal glándula La 55. Santiago) (Univ. Pérez López Miguel Adenohipófisis 54. Portugal) Lisboa. Téc. Ferreira-Dias (Univ. Graça Neurohipófisis Hipotálamo. 53. Santiago) (Univ. Pintos Casabiell Jesús endocrinología. hormonal acción de Mecanismos 52. de Santiago) (Univ. Palomino Cruz la definición de Felipe Luis y hormonas de transporte y Biosíntesis Concepto 51. 8- 18 -

FISIOLOGÍA. Boletín informativo de la SECF oéEii eoeoGtérz(nv aaoa Zaragoza) (Univ. Gutiérrez Mesonero Emilio José calor de generación y energético Metabolismo 76. Silanes de López Murillo Divina Coordinadora: Mª TERMORREGULACIÓN X: PARTE (UCM) Álvarez Arias María puesta la de Fisiología Reproducción aviar. 75. (UCM) González Lorenzo Pedro laboratorio de animales Reproducción en 74. (UCM) Rodríguez Hernández V. Medardo gatos y perros Reproducción en 73. Murcia) (Univ. López Ruiz Salvador porcinos Reproducción en 72. Murcia) (Univ. Parra Matás Carmen cabras y ovejas Reproducción en 71. México) na. Autón. Metropolita- (U. Izquierdo Córdova Alejandro bóvidos Reproducción en 70. Córdoba) (Univ. Rodríguez Vivo Rafael equinos Reproducción en 69. Madrid) Complutense (Univ. Ocejo Prieto Dolores lactación la de Fisiología 68. Complutense Madrid) (Univ. Sacristán García Albino parto del Fisiología 67. Santiago) (Univ. Palomino Cruz la de Felipe Luis gestación la de Fisiología 66. Aires) Buenos (Univ. Barbará Chiappe Angelina hembra la reproducción en la fisiológicas de Bases 65. rnic atjnMniao(nv ódb) Córdoba) (Univ. Montijano el Castejón Francisco y física de forma estado y ejercicio al tolerancia ejercicio la de Evaluación 82. del Córdoba) (Univ. Juzado Muñoz Ana neuroendocrina entrenamiento Reg. al y 81. Córdoba) ejercicio (Univ. Juzado Muñoz Ana al locomoción musculares la entrenamiento. de Biomecánica Adaptaciones 80. Argentina) Plata. la de Nac. (Univ. Trigo I. Pablo y cardiovasculares ejercicio respiratorias al hematológicas, Respuestas 79. Córdoba) (Univ. Montijano Castejón Francisco caballo el en ejercicio del energéticas Bases 78. Montijano Castejón Coordinador: Francisco corporal. EJERCICIO DEL FISIOLOGÍA XI: PARTE temperatura la Zaragoza) (Univ. Gutiérrez Mesonero Emilio José de acomodación y Adaptación Regulación 77. 9- 19 -

FISIOLOGÍA. Boletín informativo de la SECF