NEUROTROPHINS: Roles in Neuronal Development and Function
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Cell Cycle Regulation of Proliferation Versus Differentiation in the Central Nervous System
Cell Tissue Res DOI 10.1007/s00441-014-1895-8 REVIEW Cell cycle regulation of proliferation versus differentiation in the central nervous system Laura J. A. Hardwick & Fahad R. Ali & Roberta Azzarelli & Anna Philpott Received: 4 February 2014 /Accepted: 10 April 2014 # The Author(s) 2014. This article is published with open access at Springerlink.com Abstract Formation of the central nervous system requires a precise coordination and the ultimate division versus differenti- period of extensive progenitor cell proliferation, accompanied ation decision. or closely followed by differentiation; the balance between these two processes in various regions of the central nervous system Keywords Cell cycle . Differentiation . Neurogenesis . gives rise to differential growth and cellular diversity. The Proneural . Central nervous system correlation between cell cycle lengthening and differentiation has been reported across several types of cell lineage and from diverse model organisms, both in vivo and in vitro. Introduction Furthermore, different cell fates might be determined during different phases of the preceding cell cycle, indicating direct cell During development of the central nervous system (CNS), a cycle influences on both early lineage commitment and terminal period of extensive proliferation is needed to generate the re- cell fate decisions. Significant advances have been made in the quired number of progenitor cells for correct tissue and organ last decade and have revealed multi-directional interactions formation. This must be accompanied or closely followed by cell between the molecular machinery regulating the processes of differentiation, in order to generate the range of functional neu- cell proliferation and neuronal differentiation. Here, we first rons and glial cells at the correct time and place. -
Neurod1 Regulates Survival and Migration of Neuroendocrine Lung Carcinomas Via Signaling Molecules Trkb and NCAM
NeuroD1 regulates survival and migration of neuroendocrine lung carcinomas via signaling molecules TrkB and NCAM Jihan K. Osbornea, Jill E. Larsenb, Misty D. Shieldsb, Joshua X. Gonzalesa, David S. Shamesb,1, Mitsuo Satob,2, Ashwinikumar Kulkarnia,3, Ignacio I. Wistubac, Luc Girarda,b, John D. Minnaa,b, and Melanie H. Cobba,4 aDepartment of Pharmacology and bHamon Cancer Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, TX 75390-9041; and cDepartment of Translational Molecular Pathology, University of Texas MD Anderson Cancer Center, Houston, TX 77030 Contributed by Melanie H. Cobb, March 4, 2013 (sent for review February 8, 2013) Small-cell lung cancer and other aggressive neuroendocrine can- and prostate cancers, and pituitary adenomas (10–16). To charac- cers are often associated with early dissemination and frequent terize the mechanisms of NeuroD1 action in lung tumor patho- metastases. We demonstrate that neurogenic differentiation genesis, we analyzed a panel of lung cell lines. HBEC cell lines, 1 (NeuroD1) is a regulatory hub securing cross talk among survival assigned a number to distinguish lines from different individuals, and migratory-inducing signaling pathways in neuroendocrine are immortalized by overexpression of cyclin-dependent kinase 4, lung carcinomas. We find that NeuroD1 promotes tumor cell and human telomerase reverse transcriptase (e.g., HBEC3KT) (17). survival and metastasis in aggressive neuroendocrine lung tumors The immortalized HBEC3KT cell line was sequentially trans- through regulation of the receptor tyrosine kinase tropomyosin- formed by knockdown of the tumor suppressor p53 and expression related kinase B (TrkB). Like TrkB, the prometastatic signaling of K-RasV12 (HBEC3KTRL53) (Table S1) (18, 19). -
Role of Bmp4 in Female Reproductive Tract
MECHANISMS OF STRUCTURAL PLASTICITY IN MATURE SENSORY AXONS: ROLE OF BMP4 IN FEMALE REPRODUCTIVE TRACT By Aritra Bhattacherjee Submitted to the graduate degree program in Molecular and Integrative Physiology and the Graduate Faculty of the University of Kansas in partial fulfillment of requirements for the degree of Doctor of Philosophy. ________________________________ Peter G. Smith, Ph.D., Chairman ________________________________ Nancy Berman, Ph.D. ________________________________ Kenneth E. McCarson, Ph.D. ________________________________ Hiroshi Nishimune, Ph.D. ________________________________ Douglas Wright, Ph.D. Date Defended: 03/01/13 The Dissertation Committee for Aritra Bhattacherjee certifies that this is the approved version of the following dissertation: MECHANISMS OF STRUCTURAL PLASTICITY IN MATURE SENSORY AXONS: ROLE OF BMP4 IN FEMALE REPRODUCTIVE TRACT ________________________________ Peter G. Smith, PhD., Chairperson. Date approved: 03/01/13 ii ABSTRACT Structural changes in sensory axons are associated with many peripheral nerve disorders. Degenerative loss or excessive sprouting of axons are hallmarks of sensory neuropathies or hyperinnervating pain syndromes respectively. While much is known about mechanisms of developmental axon growth or regenerative outgrowth following nerve injury, there is little information about mechanisms that can induce plasticity in intact adult axons. Lack of model systems, where extensive plasticity can be predictably induced under physiological conditions, has been a fundamental impediment in studying sensory neuroplasticity mechanisms in adult. The female reproductive tract presents a highly tractable model where sensory axons cyclically undergo extensive plasticity under the influence of estrogen. In rat, high estrogen levels induce reduction in vaginal sensory nerve density, and low estrogen conditions promote sprouting leading to hyperinnervation. We used this model to explore potential factors that can initiate spontaneous plasticity in intact sensory axons. -
Identification of a Mutation in Synapsin I, a Synaptic Vesicle Protein, in a Family with Epilepsy J Med Genet: First Published As on 1 March 2004
183 SHORT REPORT Identification of a mutation in synapsin I, a synaptic vesicle protein, in a family with epilepsy J Med Genet: first published as on 1 March 2004. Downloaded from C C Garcia, H J Blair, M Seager, A Coulthard, S Tennant, M Buddles, A Curtis, J A Goodship ............................................................................................................................... J Med Genet 2004;41:183–187. doi: 10.1136/jmg.2003.013680 hippocampal bodies are moderately atrophic but without A four generation family is described in which some men of signal intensities. normal intelligence have epilepsy and others have various III-2 is a 64 year old man who has had a cerebrovascular combinations of epilepsy, learning difficulties, macrocephaly, accident but was previously of normal intelligence. He had and aggressive behaviour. As the phenotype in this family is tonic-clonic seizures until aged 7. His head circumference is distinct from other X linked recessive disorders linkage studies normal. were carried out. Linkage analysis was done using X III-3 is a 53 year old man with a full scale IQ that has been chromosome microsatellite polymorphisms to define the formally assessed as 72 (with the recognised error in such interval containing the causative gene. Genes from within assessments this places him within the borderline to mild the region were considered possible candidates and one of learning difficulties range). His head circumference is these, SYN1, was screened for mutations by direct DNA normal. As a teenager, he showed extreme physical aggres- sequencing of amplified products. Microsatellite analysis sion (he was held in a high security psychiatric hospital showed that the region between MAOB (Xp11.3) and between the ages of 11 and 18). -
Synuclein Reduces Neurotransmitter Release by Inhibiting Synaptic Vesicle Reclustering After Endocytosis
Neuron Article Increased Expression of a-Synuclein Reduces Neurotransmitter Release by Inhibiting Synaptic Vesicle Reclustering after Endocytosis Venu M. Nemani,1 Wei Lu,2 Victoria Berge,3 Ken Nakamura,1 Bibiana Onoa,1 Michael K. Lee,4 Farrukh A. Chaudhry,3 Roger A. Nicoll,2 and Robert H. Edwards1,* 1Departments of Neurology and Physiology, Graduate Program in Neuroscience 2Department of Cellular and Molecular Pharmacology University of California, San Francisco, San Francisco, CA 94158, USA 3The Biotechnology Centre of Oslo, Centre for Molecular Biology and Neuroscience, University of Oslo, Oslo, Norway 4Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA *Correspondence: [email protected] DOI 10.1016/j.neuron.2009.12.023 SUMMARY Parkinson’s disease (PD) and Lewy body dementia (LBD) (Spill- antini et al., 1998; Dickson, 2001). Point mutations in asyn are The protein a-synuclein accumulates in the brain of also linked to an autosomal-dominant form of PD (Polymeropou- patients with sporadic Parkinson’s disease (PD), los et al., 1997; Kru¨ ger et al., 1998; Zarranz et al., 2004). Taken and increased gene dosage causes a severe, domi- together, these observations suggest a causative role for asyn nantly inherited form of PD, but we know little about in sporadic as well as inherited PD and LBD. In addition, duplica- the effects of synuclein that precede degeneration. tion and triplication of the asyn gene suffice to cause a severe, a-Synuclein localizes to the nerve terminal, but the highly penetrant form of PD (Singleton et al., 2003; Chartier- Harlin et al., 2004), and polymorphisms in regulatory elements knockout has little if any effect on synaptic transmis- of the asyn gene predispose to PD (Maraganore et al., 2006), sion. -
A Novel Method of Neural Differentiation of PC12 Cells by Using Opti-MEM As a Basic Induction Medium
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 41: 195-201, 2018 A novel method of neural differentiation of PC12 cells by using Opti-MEM as a basic induction medium RENDONG HU1*, QIAOYU CAO2*, ZHONGQING SUN3, JINYING CHEN4, QING ZHENG2 and FEI XIAO1 1Department of Pharmacology, School of Medicine, Jinan University; 2College of Pharmacy, Jinan University, Guangzhou, Guangdong 510632; 3Department of Anesthesia and Intensive Care, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong 999077, SAR; 4Department of Ophthalmology, The First Clinical Medical College of Jinan University, Guangzhou, Guangdong 510632, P.R. China Received April 5, 2017; Accepted October 11, 2017 DOI: 10.3892/ijmm.2017.3195 Abstract. The PC12 cell line is a classical neuronal cell model Introduction due to its ability to acquire the sympathetic neurons features when deal with nerve growth factor (NGF). In the present study, The PC12 cell line is traceable to a pheochromocytoma from the authors used a variety of different methods to induce PC12 the rat adrenal medulla (1-4). When exposed to nerve growth cells, such as Opti-MEM medium containing different concen- factor (NGF), PC12 cells present an observable change in trations of fetal bovine serum (FBS) and horse serum compared sympathetic neuron phenotype and properties. Neural differ- with RPMI-1640 medium, and then observed the neurite length, entiation of PC12 has been widely used as a neuron cell model differentiation, adhesion, cell proliferation and action poten- in neuroscience, such as in the nerve injury-induced neuro- tial, as well as the protein levels of axonal growth-associated pathic pain model (5) and nitric oxide-induced neurotoxicity protein 43 (GAP-43) and synaptic protein synapsin-1, among model (6). -
Molecular Mediators of Acute and Chronic Itch in Mouse and Human Sensory Neurons Manouela Valtcheva Washington University in St
Washington University in St. Louis Washington University Open Scholarship Arts & Sciences Electronic Theses and Dissertations Arts & Sciences Spring 5-15-2018 Molecular Mediators of Acute and Chronic Itch in Mouse and Human Sensory Neurons Manouela Valtcheva Washington University in St. Louis Follow this and additional works at: https://openscholarship.wustl.edu/art_sci_etds Part of the Neuroscience and Neurobiology Commons Recommended Citation Valtcheva, Manouela, "Molecular Mediators of Acute and Chronic Itch in Mouse and Human Sensory Neurons" (2018). Arts & Sciences Electronic Theses and Dissertations. 1596. https://openscholarship.wustl.edu/art_sci_etds/1596 This Dissertation is brought to you for free and open access by the Arts & Sciences at Washington University Open Scholarship. It has been accepted for inclusion in Arts & Sciences Electronic Theses and Dissertations by an authorized administrator of Washington University Open Scholarship. For more information, please contact [email protected]. WASHINGTON UNIVERSITY IN ST. LOUIS Division of Biology and Biomedical Sciences Neurosciences Dissertation Examination Committee: Robert W. Gereau, IV, Chair Yu-Qing Cao Sanjay Jain Qin Liu Durga Mohapatra Molecular Mediators of Acute and Chronic Itch in Mouse and Human Sensory Neurons by Manouela Vesselinova Valtcheva A dissertation presented to The Graduate School of Washington University in partial fulfillment of the requirements for the degree of Doctor of Philosophy May 2018 St. Louis, Missouri © 2018, Manouela V. Valtcheva Table -
Angiocrine Endothelium: from Physiology to Cancer Jennifer Pasquier1,2*, Pegah Ghiabi2, Lotf Chouchane3,4,5, Kais Razzouk1, Shahin Rafi3 and Arash Rafi1,2,3
Pasquier et al. J Transl Med (2020) 18:52 https://doi.org/10.1186/s12967-020-02244-9 Journal of Translational Medicine REVIEW Open Access Angiocrine endothelium: from physiology to cancer Jennifer Pasquier1,2*, Pegah Ghiabi2, Lotf Chouchane3,4,5, Kais Razzouk1, Shahin Rafi3 and Arash Rafi1,2,3 Abstract The concept of cancer as a cell-autonomous disease has been challenged by the wealth of knowledge gathered in the past decades on the importance of tumor microenvironment (TM) in cancer progression and metastasis. The sig- nifcance of endothelial cells (ECs) in this scenario was initially attributed to their role in vasculogenesis and angiogen- esis that is critical for tumor initiation and growth. Nevertheless, the identifcation of endothelial-derived angiocrine factors illustrated an alternative non-angiogenic function of ECs contributing to both physiological and pathological tissue development. Gene expression profling studies have demonstrated distinctive expression patterns in tumor- associated endothelial cells that imply a bilateral crosstalk between tumor and its endothelium. Recently, some of the molecular determinants of this reciprocal interaction have been identifed which are considered as potential targets for developing novel anti-angiocrine therapeutic strategies. Keywords: Angiocrine, Endothelium, Cancer, Cancer microenvironment, Angiogenesis Introduction of blood vessels in initiation of tumor growth and stated Metastatic disease accounts for about 90% of patient that in the absence of such angiogenesis, tumors can- mortality. Te difculty in controlling and eradicating not expand their mass or display a metastatic phenotype metastasis might be related to the heterotypic interaction [7]. Based on this theory, many investigators assumed of tumor and its microenvironment [1]. -
Artemin, a Novel Member of the GDNF Ligand Family, Supports Peripheral and Central Neurons and Signals Through the GFR␣3–RET Receptor Complex
CORE Metadata, citation and similar papers at core.ac.uk Provided by Elsevier - Publisher Connector Neuron, Vol. 21, 1291±1302, December, 1998, Copyright 1998 by Cell Press Artemin, a Novel Member of the GDNF Ligand Family, Supports Peripheral and Central Neurons and Signals through the GFRa3±RET Receptor Complex Robert H. Baloh,* Malu G. Tansey,² et al., 1998; Milbrandt et al., 1998; reviewed by Grondin Patricia A. Lampe,² Timothy J. Fahrner,* and Gash, 1998). However, the GDNF ligands also influ- Hideki Enomoto,* Kelli S. Simburger,* ence a broad spectrum of other neuronal populations Melanie L. Leitner,² Toshiyuki Araki,* in both the CNS and PNS. GDNF and NTN both support Eugene M. Johnson, Jr.,² the survival of many peripheral neurons in culture, in- and Jeffrey Milbrandt*³ cluding sympathetic, parasympathetic, sensory, and en- *Department of Pathology and teric neurons (Buj-Bello et al., 1995; Ebendal et al., 1995; Department of Internal Medicine Trupp et al., 1995; Kotzbauer et al., 1996; Heuckeroth ² Department of Neurology and et al., 1998). In contrast, PSP does not share any of Department of Molecular Biology these peripheral activities but does support the survival and Pharmacology of dopaminergic midbrain neurons and motor neurons Washington University (Milbrandt et al., 1998). Despite the fact that GDNF acts School of Medicine on many cell populations in vitro, analysis of GDNF St. Louis, Missouri 63110 knockout mice revealed that the major developmental importance of GDNF is in the enteric nervous system and in kidney organogenesis, both of which are lost in Summary GDNF null mice (Moore et al., 1996; Pichel et al., 1996; Sanchez et al., 1996). -
Identification of Potential Key Genes and Pathway Linked with Sporadic Creutzfeldt-Jakob Disease Based on Integrated Bioinformatics Analyses
medRxiv preprint doi: https://doi.org/10.1101/2020.12.21.20248688; this version posted December 24, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. Identification of potential key genes and pathway linked with sporadic Creutzfeldt-Jakob disease based on integrated bioinformatics analyses Basavaraj Vastrad1, Chanabasayya Vastrad*2 , Iranna Kotturshetti 1. Department of Biochemistry, Basaveshwar College of Pharmacy, Gadag, Karnataka 582103, India. 2. Biostatistics and Bioinformatics, Chanabasava Nilaya, Bharthinagar, Dharwad 580001, Karanataka, India. 3. Department of Ayurveda, Rajiv Gandhi Education Society`s Ayurvedic Medical College, Ron, Karnataka 562209, India. * Chanabasayya Vastrad [email protected] Ph: +919480073398 Chanabasava Nilaya, Bharthinagar, Dharwad 580001 , Karanataka, India NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice. medRxiv preprint doi: https://doi.org/10.1101/2020.12.21.20248688; this version posted December 24, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. Abstract Sporadic Creutzfeldt-Jakob disease (sCJD) is neurodegenerative disease also called prion disease linked with poor prognosis. The aim of the current study was to illuminate the underlying molecular mechanisms of sCJD. The mRNA microarray dataset GSE124571 was downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were screened. -
Intravitreal Co-Administration of GDNF and CNTF Confers Synergistic and Long-Lasting Protection Against Injury-Induced Cell Death of Retinal † Ganglion Cells in Mice
cells Article Intravitreal Co-Administration of GDNF and CNTF Confers Synergistic and Long-Lasting Protection against Injury-Induced Cell Death of Retinal y Ganglion Cells in Mice 1, 1, 1 2 2 Simon Dulz z , Mahmoud Bassal z, Kai Flachsbarth , Kristoffer Riecken , Boris Fehse , Stefanie Schlichting 1, Susanne Bartsch 1 and Udo Bartsch 1,* 1 Department of Ophthalmology, Experimental Ophthalmology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany; [email protected] (S.D.); [email protected] (M.B.); kaifl[email protected] (K.F.); [email protected] (S.S.); [email protected] (S.B.) 2 Research Department Cell and Gene Therapy, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany; [email protected] (K.R.); [email protected] (B.F.) * Correspondence: [email protected]; Tel.: +49-40-7410-55945 A first draft of this manuscript is part of the unpublished doctoral thesis of Mahmoud Bassal. y Shared first authorship. z Received: 9 August 2020; Accepted: 9 September 2020; Published: 11 September 2020 Abstract: We have recently demonstrated that neural stem cell-based intravitreal co-administration of glial cell line-derived neurotrophic factor (GDNF) and ciliary neurotrophic factor (CNTF) confers profound protection to injured retinal ganglion cells (RGCs) in a mouse optic nerve crush model, resulting in the survival of ~38% RGCs two months after the nerve lesion. Here, we analyzed whether this neuroprotective effect is long-lasting and studied the impact of the pronounced RGC rescue on axonal regeneration. To this aim, we co-injected a GDNF- and a CNTF-overexpressing neural stem cell line into the vitreous cavity of adult mice one day after an optic nerve crush and determined the number of surviving RGCs 4, 6 and 8 months after the lesion. -
Effects of PACAP on Schwann Cells
International Journal of Molecular Sciences Review Effects of PACAP on Schwann Cells: Focus on Nerve Injury 1, 2, 1 3 Grazia Maugeri y, Agata Grazia D’Amico y, Giuseppe Musumeci , Dora Reglodi and Velia D’Agata 1,* 1 Department of Biomedical and Biotechnological Sciences, Section of Anatomy, Histology and Movement Sciences, University of Catania, 95100 Catania, Italy; [email protected] (G.M.); [email protected] (G.M.) 2 Department of Drug Sciences, University of Catania, 95100 Catania, Italy; [email protected] 3 Department of Anatomy, MTA-PTE PACAP Research Team, University of Pécs Medical School, Szigeti út 12, H-7624 Pécs, Hungary; [email protected] * Correspondence: [email protected]; Tel.: +39-095-3782039 These authors contributed equally to this work. y Received: 29 September 2020; Accepted: 2 November 2020; Published: 3 November 2020 Abstract: Schwann cells, the most abundant glial cells of the peripheral nervous system, represent the key players able to supply extracellular microenvironment for axonal regrowth and restoration of myelin sheaths on regenerating axons. Following nerve injury, Schwann cells respond adaptively to damage by acquiring a new phenotype. In particular, some of them localize in the distal stump to form the Bungner band, a regeneration track in the distal site of the injured nerve, whereas others produce cytokines involved in recruitment of macrophages infiltrating into the nerve damaged area for axonal and myelin debris clearance. Several neurotrophic factors, including pituitary adenylyl cyclase-activating peptide (PACAP), promote survival and axonal elongation of injured neurons. The present review summarizes the evidence existing in the literature demonstrating the autocrine and/or paracrine action exerted by PACAP to promote remyelination and ameliorate the peripheral nerve inflammatory response following nerve injury.