DOCSLIB.ORG

Anti-Inflammatory Immune Regulation

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Anti-Inflammatory Immune Regulation Surfactant Protein A Activation of Atypical Protein Kinase C ζ in IκB-α-Dependent Anti-Inflammatory Immune Regulation This information is current as Christina Moulakakis, Stefanie Adam, Ulrike Seitzer, Andra of September 29, 2021. B. Schromm, Michael Leitges and Cordula Stamme J Immunol 2007; 179:4480-4491; ; doi: 10.4049/jimmunol.179.7.4480 http://www.jimmunol.org/content/179/7/4480 Downloaded from References This article cites 61 articles, 32 of which you can access for free at: http://www.jimmunol.org/content/179/7/4480.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on September 29, 2021 *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2007 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Surfactant Protein A Activation of Atypical Protein Kinase C ␨ in I␬B-␣-Dependent Anti-Inflammatory Immune Regulation1 Christina Moulakakis,* Stefanie Adam,* Ulrike Seitzer,† Andra B. Schromm,‡ Michael Leitges,§ and Cordula Stamme2*¶ The pulmonary collectin surfactant protein (SP)-A has a pivotal role in anti-inflammatory modulation of lung immunity. The mechanisms underlying SP-A-mediated inhibition of LPS-induced NF-␬B activation in vivo and in vitro are only partially un- derstood. We previously demonstrated that SP-A stabilizes I␬B-␣, the primary regulator of NF-␬B, in alveolar macrophages (AM) both constitutively and in the presence of LPS. In this study, we show that in AM and PBMC from I␬B-␣ knockout/I␬B-␤ knockin mice, SP-A fails to inhibit LPS-induced TNF-␣ production and p65 nuclear translocation, confirming a critical role for I␬B-␣ in SP-A-mediated LPS inhibition. We identify atypical (a) protein kinase C (PKC) ␨ as a pivotal upstream regulator of SP-A- ؊ ؊ mediated I␬B-␣/NF-␬B pathway modulation deduced from blocking experiments and confirmed by using AM from PKC␨ / Downloaded from mice. SP-A transiently triggers aPKCThr410/403 phosphorylation, aPKC kinase activity, and translocation in primary rat AM. Coimmunoprecipitation experiments reveal that SP-A induces aPKC/p65 binding under constitutive conditions. Together the data indicate that anti-inflammatory macrophage activation via I␬B-␣ by SP-A critically depends on PKC␨ activity, and thus attribute a novel, stimulus-specific signaling function to PKC␨ in SP-A-modulated pulmonary immune response. The Journal of Immu- nology, 2007, 179: 4480–4491. http://www.jimmunol.org/ ulmonary surfactant is a lipid-protein complex that con- Alveolar macrophages (AM), normally accounting for ϳ95% of stitutes the alveolar liquid layer of the lung. The unique airspace leukocytes, are a unique class of professional phagocytes P composition of surfactant facilitates the functional combi- that represent the major effector cells of the pulmonary innate im- nation of different biological effects such as preventing alveolar mune system (6). SP-A directly interacts with AM through binding collapsing at expiration and immunomodulating innate pulmonary to cell surface receptors, resulting in modulation of chemotaxis, host defense responses (1, 2). The latter function is primarily me- phagocytosis, and modified pro- or anti-inflammatory immune re- diated by surfactant proteins (SP)3-A and SP-D belonging to the sponses (7). collectin family. SP-A, the most abundant pulmonary collectin, LPS, the main component of the outer leaflet of the outer by guest on September 29, 2021 binds and aggregates a variety of microorganisms and enhances membrane of Gram-negative bacteria, substantially contributes their phagocytosis and killing both in vivo and in vitro (3). SP-A- to the pathophysiology of the most frequent lung diseases, in- deficient mice exhibit delayed microbial clearance and higher lev- cluding pneumonia, acute lung injury, and acute respiratory dis- els of bronchoalveolar inflammatory mediators after intratracheal tress syndrome (8). Whereas LPS recognition benefits the host inoculation with a variety of clinically relevant pathogens (4), as by sensing bacteria and mobilizing defense mechanisms, an ex- well as to isolated LPS (5). aggerated response to LPS contributes to the development of a local or systemic septic shock syndrome. The interaction of picomolar concentrations of LPS with a receptor complex in- cluding TLR4, MD-2, LPS-binding protein, and CD14 on host *Department of Immunochemistry and Biochemical Microbiology, Division of Cel- cells initiates the sequential activation of multiple signaling lular Pneumology, Research Center Borstel, Leibniz Center for Medicine and Bio- ␬ science, Borstel, Germany; †Department of Immunology and Cell Biology, Division pathways, including NF- B, a central regulator of LPS-medi- of Veterinary Infection Biology and Immunology, Research Center Borstel, Leibniz ated cell activation (9–11). ‡ Center for Medicine and Bioscience, Borstel, Germany; Emmy-Noether Group Im- The most prominent NF-␬B heterodimer p65/p50 is sequestered munobiophysics, Research Center Borstel, Leibniz Center for Medicine and Bio- science, Borstel, Germany; §Biotechnolgy Centre of Oslo, University of Oslo, Oslo, in the cytoplasm by a family of inhibitory proteins, among Norway; and ¶Department of Anesthesiology, University Hospital of Lu¨beck, Lu¨- which I␬B-␣ is the best characterized and assumed to function beck, Germany as the primary regulator of NF-␬B in both stimulated and rest- Received for publication February 15, 2007. Accepted for publication July 30, 2007. ing cells (12, 13). In response to many stimuli including LPS, The costs of publication of this article were defrayed in part by the payment of page ␬ ␣ ␬ charges. This article must therefore be hereby marked advertisement in accordance I B- becomes degraded via ubiquitination in an I B kinase with 18 U.S.C. Section 1734 solely to indicate this fact. (IKK)-dependent manner (12, 14, 15). The removal of I␬B-␣ 1 This work was supported by the Deutsche Forschungsgemeinschaft 609/1-3 and allows the nuclear translocation of NF-␬B and subsequently the 609/1-4 (to C.S.) and 621/2-2 (to A.B.S.). transcription of downstream target genes, including I␬B-␣ itself 2 Address correspondence and reprint requests to Dr. Cordula Stamme, Research (16). Secondary clues point to an I␬B-independent pathway, Center Borstel, Parkallee 22, D-23845 Borstel, Germany. E-mail address: ␬ [email protected] and include the phosphorylation of p65 to activate NF- B- dependent gene transcription (17). 3 Abbreviations used in this paper: SP, surfactant protein; AKBI, I␬B-␣ knockout/ I␬B-␤ knockin; AM, alveolar macrophage; aPKC, atypical protein kinase C; cPKC, SP-A has been shown to inhibit LPS-induced TNF-␣ production classical protein kinase C; DAG, diacylglycerol; HI, heat inactivated; IKK, I␬B ki- (18–21), inducible NO synthase protein expression (22), NF-␬B ac- nase; PKC, protein kinase C; ps, pseudosubstrate; wt, wild type. tivity (20, 23, 24), and, upon diverse stimuli, NADPH oxidase (25) in Copyright © 2007 by The American Association of Immunologists, Inc. 0022-1767/07/$2.00 immunocompetent cells. We recently demonstrated that SP-A exerts www.jimmunol.org The Journal of Immunology 4481 its anti-inflammatory effects on LPS-challenged AM via a mechanism 37°C in a 5% CO2 atmosphere. Then the medium was changed and the involving a SP-A-mediated direct modulation of the basal and LPS- cells were treated with SP-A (20–60 ␮g/ml) and/or LPS (10–100 ng/ml) coupled I␬B-␣ turnover in these cells (24). In that study, SP-A in- for indicated times at 37°C in the presence of 0.2% heat-inactivated (HI) ␬ ␣ FCS. In separate experiments, AM were treated with a panel of kinase creased I B- protein expression in a dose- and time-dependent man- inhibitors to determine their possible effect on I␬B-␣ protein expression as ner without inducing I␬B-␣ phosphorylation or I␬B-␣ mRNA levels follows: Go¨-6976 (5 ␮M), Go¨-6850 (5 nM), chelerythrine chloride (6 and both basal and in the presence of LPS. However, the signaling path- 12 ␮M), or aPKCps peptides (2, 5, and 10 ␮M) were used to inhibit distinct ways controlling the SP-A-mediated attenuation of LPS-induced subsets of cPKC, novel PKC, or aPKCs. Wortmannin (50 nM) was used as PI3K inhibitor, and apigenin (30 ␮M) to inhibit protein kinase CKII. proinflammatory signals via I␬B-␣ remain unknown. A role for individual members of the protein kinase C (PKC) Nuclear protein extraction ␬ ␣ family in both SP-A immune modulation (26) and I B- turnover After treatment, cells were scraped off with 500 ␮l of cold PBS and spun (27) has been suggested previously. PKC family members are ex- at 4,500 ϫ g, 5 min, 4°C. The resulting pellet was resuspended in 400 ␮l pressed in many different cell types, in which they regulate a wide of ice-cold buffer A (10 mM Tris, 5 mM MgCl2,10mMKCl,1mM variety of cellular processes such as cell differentiation, cytoskel- ethyleneglycol-bis-(2-aminoethyl ether)-N,N,NЈ,NЈ-tetraacetic acid, 0.3 M ␤ etal remodeling, and gene expression in response to diverse stimuli sucrose, 1 mM DTT, 10 mM -glycerol phosphate, 0.5 mM PMSF, and 1.5 ␮l of protease inhibitor mixture (Complete; Roche)) and incubated on ice (28, 29). Based on sequence homology and the mechanism of their for 15 min; 25 ␮l of 10% Nonidet P-40 was then added and vortexed for regulation, individual members of the PKC family are subdivided 10 s.
Load more

Recommended publications
  • Draft Assessment Report on Chelidonium Majus L., Herba
    25 November 2010 EMA/HMPC/369801/2009 Committee on Herbal Medicinal Products (HMPC) Assessment report on Chelidonium majus L., herba Based on Article 10a of Directive 2001/83/EC as amended (well-established use) Based on Article 16d(1), Article 16f and Article 16h of Directive 2001/83/EC as amended (traditional use) Draft Herbal substance(s) (binomial scientific name of Chelidonium majus L. the plant, including plant part) Dried whole or cut aerial parts of the plant Herbal preparation(s) Internal Use a) Chelidonii herba: comminuted b) Chelidonii tincture: 1:10 ethanol 45% (V/V) c) Chelidonii extractum fluidum: 1:1 ethanol 25% (V/V) d) Chelidonii extractum siccum (concentration not specified) e) Chelidonium majus mother tincture (M.T. (ø)) External Use a) Eye-drops: (preparation not specified) b) Ointment: (concentration not specified) Pharmaceutical forms Herbal preparation in solid or liquid dosage form or as a herbal tea for oral use. Herbal preparation in solid or liquid dosage form for external use. Rapporteur Assessor(s) 7 Westferry Circus ● Canary Wharf ● London E14 4HB ● United Kingdom Telephone +44 (0)20 7418 8400 Facsimile +44 (0)20 7523 7051 E-mail [email protected] Website www.ema.europa.eu An agency of the European Union © European Medicines Agency, 2011. Reproduction is authorised provided the source is acknowledged. Note: This Assessment Report is published to support the release for public consultation of the draft Community herbal monograph on Chelidonium majus L. It should be noted that this document is a working document, not yet fully edited, and which shall be further developed after the release for consultation of the monograph.
    [Show full text]
  • Effects of Berberine, Chelerythrine, and Sanguinarine on Proliferation in Four Human Immortalized Cell Lines
    Journal of the Iowa Academy of Science: JIAS Volume 119 Number 1-4 Article 6 2012 Effects of Berberine, Chelerythrine, and Sanguinarine on Proliferation in Four Human Immortalized Cell Lines David S. Senchina Drake University Nisarg B. Shah Drake University Marc G. Busch Drake University Let us know how access to this document benefits ouy Copyright © Copyright 2014 by the Iowa Academy of Science, Inc. Follow this and additional works at: https://scholarworks.uni.edu/jias Part of the Anthropology Commons, Life Sciences Commons, Physical Sciences and Mathematics Commons, and the Science and Mathematics Education Commons Recommended Citation Senchina, David S.; Shah, Nisarg B.; and Busch, Marc G. (2012) "Effects of Berberine, Chelerythrine, and Sanguinarine on Proliferation in Four Human Immortalized Cell Lines," Journal of the Iowa Academy of Science: JIAS, 119(1-4), 22-27. Available at: https://scholarworks.uni.edu/jias/vol119/iss1/6 This Research is brought to you for free and open access by the Iowa Academy of Science at UNI ScholarWorks. It has been accepted for inclusion in Journal of the Iowa Academy of Science: JIAS by an authorized editor of UNI ScholarWorks. For more information, please contact [email protected]. Jour. Iowa Acad. Sci. 119(1--4):22-27, 2012 Effects of Berberine, Chelerythrine, and Sanguinarine on Proliferation in Four Human Immortalized Cell Lines DAVIDS. SENCHINA1·*, NISARG B. SHAH2 and MARC G. BUSCH 1 1Deparcmenc of Biology, Drake University, Des Moines, IA 2Pharmacy Program, Drake University, Des Moines, IA Bloodroot (Sanguinaria canadensis L., Papaveraceae) is a plane rich in benzophenanchridine (isoquinoline) alkaloids ~uch_ as sanguinarine and chelerychrine.
    [Show full text]
  • Consecutive Pharmacological Activation of PKA and PKC Mimics the Potent Cardioprotection of Temperature Preconditioning
    Cardiovascular Research (2010) 88, 324–333 doi:10.1093/cvr/cvq190 Consecutive pharmacological activation of PKA and PKC mimics the potent cardioprotection of temperature preconditioning Igor Khaliulin*, Joanna E. Parker, and Andrew P. Halestrap Department of Biochemistry and the Bristol Heart Institute, University of Bristol, University Walk, Bristol BS8 1TD, UK Received 18 February 2010; revised 14 May 2010; accepted 8 June 2010; online publish-ahead-of-print 16 June 2010 Time for primary review: 25 days Aims Temperature preconditioning (TP) provides very powerful protection against ischaemia/reperfusion. Understanding the signalling pathways involved may enable the development of effective pharmacological cardioprotection. We investigated the interrelationship between activation of protein kinase A (PKA) and protein kinase C (PKC) in the signalling mechanisms of TP and developed a potent pharmacological intervention based on this mechanism. ..................................................................................................................................................................................... Methods Isolated rat hearts were subjected to TP, 30 min global ischaemia, and 60 min reperfusion. Other control and TP and results hearts were perfused with either sotalol (b-adrenergic blocker) or H-89 (PKA inhibitor). Some hearts were pre- treated with either isoproterenol (b-adrenergic agonist) or adenosine (PKC activator) that were given alone, simul- taneously, or sequentially. Pre-treatment with isoproterenol,
    [Show full text]
  • Recognition of Chelerythrine to Human Telomeric DNA and RNA G
    OPEN Recognition of Chelerythrine to Human SUBJECT AREAS: Telomeric DNA and RNA DNA NUCLEIC ACIDS G-quadruplexes Li-Ping Bai1, Masaki Hagihara2, Kazuhiko Nakatani2 & Zhi-Hong Jiang1 Received 19 June 2014 1State Key Laboratory of Quality Research in Chinese Medicine, and Macau Institute for Applied Research in Medicine and Health, Accepted Macau University of Science and Technology, Macau, 2Regulatory Bioorganic Chemistry, The Institute of Scientific and Industrial 29 September 2014 Research (SANKEN), Osaka University, Japan. Published 24 October 2014 A study on binding of antitumor chelerythrine to human telomeric DNA/RNA G-quadruplexes was performed by using DNA polymerase stop assay, UV-melting, ESI-TOF-MS, UV-Vis absorption spectrophotometry and fluorescent triazole orange displacement assay. Chelerythrine selectively binds to and stabilizes the K1-form hybrid-type human telomeric DNA G-quadruplex of biological significance, Correspondence and compared with the Na1-form antiparallel-type DNA G-quadruplex. ESI-TOF-MS study showed that requests for materials chelerythrine possesses a binding strength for DNA G-quadruplex comparable to that of TMPyP4 should be addressed to tetrachloride. Both 151 and 251 stoichiometries were observed for chelerythrine’s binding with DNA and Z.-H.J. (zhjiang@must. RNA G-quadruplexes. The binding strength of chelerythrine with RNA G-quadruplex is stronger than that edu.mo) with DNA G-quadruplex. Fluorescent triazole orange displacement assay revealed that chelerythrine interacts with human telomeric RNA/DNA G-quadruplexes by the mode of end- stacking. The relative binding strength of chelerythrine for human telomeric RNA and DNA G-quadruplexes obtained from ESI-TOF-MS experiments are respectively 6.0- and 2.5-fold tighter than that with human telomeric double-stranded hairpin DNA.
    [Show full text]
  • Role of Adenosine in Insulin-Stimulated Release Of
    Role of Adenosine in Insulin-Stimulated Release of Leptin From Isolated White Adipocytes of Wistar Rats Ju e i - T ang Cheng, I-Min Liu, Tzong-Cherng Chi, Kazumasa Shinozuka, Feng-Hwa Lu, Ta-Jen Wu, and Chih Jen Chang Leptin, the o b gene product that can decrease caloric intake and increase energy expenditure, is function- ally released by insulin from adipose tissue. Adenosine he ob gene, which encodes a 167-amino acid pep- is thought to be an important regulator of the action of tide named leptin in white adipocytes (1), has insulin in adipose tissue. The present study investi- received increasing attention for its role in the gated the role of adenosine in the release of leptin by regulation of food intake and whole-body energy insulin in isolated rat white adipocytes. Release of lep- T balance in rodents and humans (2,3). It has been demon- tin, measured by radioimmunoassay, from insulin-stim- ulated samples was seen after 30 min. Adenosine deam- strated that circulatory leptin levels in rats were modulated inase, at concentrations sufficient to metabolize by exogenous insulin (4) and ob gene expression was endogenous adenosine, decreased insulin-stimulated induced by corticosteroids (5). Insulin also stimulated the leptin release. Also, the insulin-stimulated leptin mRNA levels of the ob gene in rat adipocytes (6). Thus, release was completely blocked by the adenosine A1 insulin appears to be one of the important regulators of ob receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine gene expression and leptin secretion in adipose tissue. (DPCPX). Mediation of endogenous adenosine in this Adenosine is another endogenous regulator in adipose action of insulin was further supported by the assay of tissue.
    [Show full text]
  • Inhibition of Protein Kinase C Signaling Protects Prefrontal Cortex Dendritic
    Inhibition of protein kinase C signaling protects SEE COMMENTARY prefrontal cortex dendritic spines and cognition from the effects of chronic stress Avis Brennan Hainsa, Mai Anh T. Vua, Paul K. Maciejewskib,1, Christopher H. van Dycka,b, Melissa Gottrona, and Amy F. T. Arnstena,2 aDepartment of Neurobiology, Yale University School of Medicine, 333 Cedar Street SHM C-303, New Haven, CT 06510; and bDepartment of Psychiatry, Yale University School of Medicine, 300 George Street, New Haven, CT 06511 Communicated by Bruce S. McEwen, The Rockefeller University, New York, NY, August 13, 2009 (received for review April 7, 2009) The prefrontal cortex r regulates behavior, cognition, and emotion form the networks subserving representational knowledge (1), and by using working memory. Prefrontal functions are impaired by particularly in distal apical dendrites (11). However, the molecular stress exposure. Acute, stress-induced deficits arise from excessive changes underlying this spine loss are not yet understood. protein kinase C (PKC) signaling, which diminishes prefrontal It is likely that many molecular ‘‘culprits’’ contribute to architectural neuronal firing. Chronic stress additionally produces architectural changes in prefrontal neurons during chronic stress. One likely candi- changes, reducing dendritic complexity and spine density of cor- date contributing to dendritic spine loss is PKC intracellular signaling, tico-cortical pyramidal neurons, thereby disrupting excitatory as in vitro studies of hippocampal cell cultures have shown that elevated working memory networks. In vitro studies have found that PKC signaling induces spine collapse through disruption of the actin sustained PKC activity leads to spine loss from hippocampal- cytoskeleton (20). Excessive PKC signaling also has immediate clinical cultured neurons, suggesting that PKC may contribute to spine loss relevance, as either genetic or environmental insults can overactivate during chronic stress exposure.
    [Show full text]
  • Protein Kinase Inhibitors Using ALZET Osmotic Pumps
    ALZET® Bibliography References on the Administration of Protein Kinase inhibitors Using ALZET Osmotic Pumps 1. Calphostin C Q3801: P. Almela, et al. Crosstalk between G protein-coupled receptors (GPCRs) and tyrosine kinase receptor (TXR) in the heart after morphine withdrawal. FRONTIERS IN PHARMACOLOGY 2013;4(U1547-U1559HA-1004; calphostin c Agents: HA-1004; calphostin c Vehicle: Water, sterile; DMSO; Route: SC; Species: Rat; Pump: 2001; Duration: 7 days; ALZET Comments: Controls received mp w/ vehicle; animal info (male, Sprague Dawley, 220-240g); 0.06% DMSO used; dependence; cardiovascular; pumps primed for 5 hours in 37C saline; Q1721: F. Martin, et al. Protein kinase C phosphorylates the cAMP response element binding protein in the hypothalamic paraventricular nucleus during morphine withdrawal. British Journal of Pharmacology 2011;163(4):857-875 Agents: Calphostin C; chelerythrine Vehicle: Not Stated; Route: SC; Species: Rat; Pump: Not Stated; Duration: 7 days; ALZET Comments: Animal info (Sprague Dawley, male, 220-240 g); enzyme inhibitor (PKC, protein kinase C) Q0669: F. Martin, et al. Morphine withdrawal regulates phosphorylation of cAMP response element binding protein (CREB) through PKC in the nucleus tractus solitarius-A(2) catecholaminergic neurons. Journal of Neurochemistry 2009;110(5):1422-1432 Agents: Calphostin C Vehicle: Not Stated; Route: SC; Species: Rat; Pump: 2001; Duration: 7 days; ALZET Comments: Controls received mp w/ saline; animal info (male, Sprague-Dawley, 220-240 g); enzyme inhibitor (PKC, protein kinase C) Q0460: P. Almela, et al. Cross-Talk between Protein Kinase A and Mitogen-Activated Protein Kinases Signalling in the Adaptive Changes Observed during Morphine Withdrawal in the Heart.
    [Show full text]
  • In Vitro and in Vivo Effects of Flavonoids on Peripheral Neuropathic Pain
    Kinesiology and Nutrition Sciences Faculty Publications Kinesiology and Nutrition Sciences 3-5-2020 In Vitro and In Vivo Effects of Flavonoids on Peripheral Neuropathic Pain Paramita Basu University of Pittsburgh School of Medicine Arpita Basu University of Nevada, Las Vegas, [email protected] Follow this and additional works at: https://digitalscholarship.unlv.edu/kns_fac_articles Part of the Nervous System Diseases Commons, and the Pain Management Commons Repository Citation Basu, P., Basu, A. (2020). In Vitro and In Vivo Effects of Flavonoids on Peripheral Neuropathic Pain. Molecules, 25(5), 1-36. MDPI. http://dx.doi.org/10.3390/molecules25051171 This Article is protected by copyright and/or related rights. It has been brought to you by Digital Scholarship@UNLV with permission from the rights-holder(s). You are free to use this Article in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s) directly, unless additional rights are indicated by a Creative Commons license in the record and/ or on the work itself. This Article has been accepted for inclusion in Kinesiology and Nutrition Sciences Faculty Publications by an authorized administrator of Digital Scholarship@UNLV. For more information, please contact [email protected]. molecules Review In Vitro and In Vivo Effects of Flavonoids on Peripheral Neuropathic Pain Paramita Basu 1 and Arpita Basu 2,* 1 Department of Anesthesiology, Pittsburgh Center for Pain Research, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA; [email protected] 2 Department of Kinesiology and Nutrition Sciences, School of Integrated Health Sciences, University of Nevada, Las Vegas, NV 89154, USA * Correspondence: [email protected]; Tel.: +702-895-4576; Fax: +702-895-1500 Academic Editor: H.P.
    [Show full text]
  • Binding of Flavonoids to Duplex and Triplex Nucleic Acid Structures: Biophysical and Thermodynamic Approach
    Final Report of the Major Research Project. MRP-MAJOR-CHEM-2013-37991 Binding of flavonoids to duplex and triplex nucleic acid structures: Biophysical and thermodynamic approach Final Report MRP-MAJOR-CHEM-2013-37991; UGC Reference No. F. 43-243/2014(SR) By Dr. Suman Das Associate Professor Department of Chemistry (Physical Chemistry Section), Jadavpur University Raja S.C. Mullick Road, Jadavpur, Kolkata 700 032 E-mail. [email protected] Final Report of the work done on the Major Research Project. MRP-MAJOR-CHEM-2013-37991 University Grants Commission (Ministry of Human Resource and Development) Bahadur Shah Zafar Marg, New Delhi-110002 PROFORMA FOR SUBMISSION OF INFORMATION AT THE TIME OF SENDING THE FINAL REPORT OF THE WORK DONE ON THE PROJECT 1. Title of the Project : Binding of flavonoids to duplex and triplex nucleic acid structures: Biophysical and thermodynamic approach 2. Name and address of the Principal : Name: Dr. Suman Das Investigator Office: Department of Chemistry Jadavpur University, Kolkata 700 032, WB, India; Mob: 9434373164 E-mail: [email protected] 033 24572349 Res: 30/21, Baruipara 1st Bye Lane, P.O. Santragachi, Howrah 711 104, WB, India. 033 26674127 3. Name and address of the Institution : Department of Chemistry Jadavpur University, 188, Raja S C Mullick Road, Kolkata 700 032, WB, India 4. UGC Approval Letter No. and Date : No.F.43-243/2014(SR) dated 06-07-2015 5. Date of implementation : 1st July, 2015 6. Tenure of the project : 30th June, 2018 7. Total grant allocated : Rs. 12,07,674/- 8. Total grant received : Rs. 10,98,966/- 9.
    [Show full text]
  • Plant Natural Compounds with Antibacterial Activity Towards Common Pathogens of Pond-Cultured Channel Catfish (Ictalurus Punctatus)
    Toxins 2010, 2, 1676-1689; doi:10.3390/toxins2071676 OPEN ACCESS toxins ISSN 2072-6651 www.mdpi.com/journal/toxins Article Plant Natural Compounds with Antibacterial Activity towards Common Pathogens of Pond-Cultured Channel Catfish (Ictalurus punctatus) Kevin K. Schrader United States Department of Agriculture, Agricultural Research Service, Natural Products Utilization Research Unit, National Center for Natural Products Research, Post Office Box 8048, University of Mississippi, 38677, USA; E-Mail: [email protected]; Tel.: 662-915-1144; Fax: 662-915-1035 Received: 28 April 2010; in revised form: 23 June 2010 / Accepted: 25 June 2010 / Published: 28 June 2010 Abstract: The bacteria Edwardsiella ictaluri and Flavobacterium columnare cause enteric septicemia and columnaris disease, respectively, in channel catfish (Ictalurus punctatus). Natural therapeutants may provide an alternative to current management approaches used by producers. In this study, a rapid bioassay identified plant compounds as potential therapeutants. Chelerythrine chloride and ellagic acid were the most toxic toward E. ictaluri, with 24-h IC50 of 7.3 mg/L and 15.1 mg/L, respectively, and MIC of 2.1 mg/L and 6.5 mg/L, respectively. Chelerythrine chloride, ellagic acid, β-glycyrrhetinic acid, sorgoleone, and wogonin were the most toxic towards two genomovars of F. columnare, and wogonin had the strongest antibacterial activity (MIC = 0.3 mg/L). Keywords: antibacterial; channel catfish; chelerythrine; columnaris; ellagic acid; enteric septicemia of catfish; β-glycyrrhetinic acid; sorgoleone; therapeutant; wogonin 1. Introduction Enteric septicemia of catfish (ESC) is the leading cause of mortality in pond-raised channel catfish in the United States and is caused by the Gram-negative bacterium Edwardsiella ictaluri [1].
    [Show full text]
  • Role of Inositol 1,4,5-Trisphosphate Receptors in Α1-Adrenergic
    Acta Pharmacologica Sinica 2006 Jul; 27 (7): 895–900 Full-length article α Role of inositol 1,4,5-trisphosphate receptors in 1-adrenergic receptor- induced cardiomyocyte hypertrophy1 Da-li LUO2,3,5, Jian GAO2, Xiao-mei LAN3, Gang WANG4, Sheng WEI4, Rui-ping XIAO4, Qi-de HAN3 2Department of Pharmacology, School of Chemical Biology & Pharmaceutical Sciences, Capital University of Medical Sciences, Beijing 100069, China; 3Institute of Cardiovascular Science at Health Science Center, Peking University, Beijing 100083, China; 4Institute of Molecular Medicine and College of Life Science, Peking University, Beijing 100871, China Key words Abstract inositol 1,4,5-trisphosphate receptors; Ca2+ Aim: Intracellular Ca2+ plays pivotal roles in diverse cellular functions, including sparks; α adrenergic stimulation; cardiac 1 gene transcription that underlies cardiac remodeling during stress responses. hypertrophy However, the role of inositol 1,4,5-trisphosphate receptors (IP3Rs) in the media- tion of cardiac intracellular Ca2+ and hypertrophic growth remains elusive. Prior 1 Project supported by the National Natural work with neonatal rat ventricular myocytes suggests that activation of IP Rs Science Foundation of China (No 30470692). 3 α α 2+ 5 Correspondence to Dr Da-li LUO. may be linked to 1 adrenergic receptor ( 1AR) increased stereotyped Ca spark Phn 86-10-8391-1519. occurrence and global Ca2+ oscillations. Thus, we hypothesized that Ca2+ release Fax 86-10-8391-1520. through IP Rs was necessary for α AR-stimulated cardiac hypertrophy. Methods: E-mail [email protected] 3 1 We used myoinositol 1,4,5-trisphosphate hexakis (butyryloxymethyl) ester (IP3BM), Received 2006-04-18 a membrane-permeant ester of IP3, to activate IP3Rs directly, and Fluo 4/AM to Accepted 2006-05-17 2+ µ -1 measure intracellular Ca signaling.
    [Show full text]
  • Influence of Solvent Polarity and DNA-Binding on Spectral
    RESEARCH ARTICLE Influence of Solvent Polarity and DNA- Binding on Spectral Properties of Quaternary Benzo[c]phenanthridine Alkaloids Michal Rájecký1, Kristýna Šebrlová2, Filip Mravec3, Petr Táborský1,4* 1 Central European Institute of Technology (CEITEC), Masaryk University, Brno, Czech Republic, 2 Department of Biochemistry, Faculty of Medicine, Masaryk University, Brno, Czech Republic, 3 Materials Research Centre, Faculty of Chemistry, Brno University of Technology, Brno, Czech Republic, 4 Department of Chemistry, Faculty of Science, Masaryk University, Brno, Czech Republic * [email protected] Abstract Quaternary benzo[c]phenanthridine alkaloids are secondary metabolites of the plant fami- lies Papaveraceae, Rutaceae, and Ranunculaceae with anti-inflammatory, antifungal, anti- microbial and anticancer activities. Their spectral changes induced by the environment OPEN ACCESS could be used to understand their interaction with biomolecules as well as for analytical pur- poses. Spectral shifts, quantum yield and changes in lifetime are presented for the free form Citation: Rájecký M, Šebrlová K, Mravec F, of alkaloids in solvents of different polarity and for alkaloids bound to DNA. Quantum yields Táborský P (2015) Influence of Solvent Polarity and DNA-Binding on Spectral Properties of Quaternary range from 0.098 to 0.345 for the alkanolamine form and are below 0.033 for the iminium Benzo[c]phenanthridine Alkaloids. PLoS ONE 10(6): form. Rise of fluorescence lifetimes (from 2–5nsto3–10 ns) and fluorescence intensity are e0129925. doi:10.1371/journal.pone.0129925 observed after binding of the iminium form to the DNA for most studied alkaloids. The alka- Academic Editor: Heidar-Ali Tajmir-Riahi, University nolamine form does not bind to DNA.
    [Show full text]