Document Detail


In vivo analysis of Schwann cell programmed cell death in the embryonic chick: regulation by axons and glial growth factor.
MedLine Citation:
PMID:  12040058     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The present study uses the embryonic chick to examine in vivo the mechanisms and regulation of Schwann cell programmed cell death (PCD) in spinal and cranial peripheral nerves. Schwann cells are highly dependent on the presence of axons for survival because the in ovo administration of NMDA, which excitotoxically eliminates motoneurons and their axons by necrosis, results in a significant increase in apoptotic Schwann cell death. Additionally, pharmacological and surgical manipulation of axon numbers also affects the relative amounts of Schwann cell PCD. Schwann cells undergoing both normal and induced PCD display an apoptotic-like cell death, using a caspase-dependent pathway. Furthermore, axon elimination results in upregulation of the p75 and platelet-derived growth factor receptors in mature Schwann cells within the degenerating ventral root. During early development, Schwann cells are also dependent on axon-derived mitogens; the loss of axons results in a decrease in Schwann cell proliferation. Axon removal during late embryonic stages, however, elicits an increase in proliferation, as is expected from these more differentiated Schwann cells. In rodents, Schwann cell survival is regulated by glial growth factor (GGF), a member of the neuregulin family of growth factors. GGF administration to chick embryos selectively rescued Schwann cells during both normal PCD and after the loss of axons, whereas other trophic factors tested had no effect on Schwann cell survival. In conclusion, avian Schwann cells exhibit many similarities to mammalian Schwann cells in terms of their dependence on axon-derived signals during early and later stages of development.
Authors:
Adam K Winseck; Jordi Caldero; Dolors Ciutat; David Prevette; Sheryl A Scott; Gouying Wang; Josep E Esquerda; Ronald W Oppenheim
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of neuroscience : the official journal of the Society for Neuroscience     Volume:  22     ISSN:  1529-2401     ISO Abbreviation:  J. Neurosci.     Publication Date:  2002 Jun 
Date Detail:
Created Date:  2002-05-31     Completed Date:  2002-07-05     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8102140     Medline TA:  J Neurosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4509-21     Citation Subset:  IM    
Affiliation:
Department of Neurobiology and Anatomy and Neuroscience Program, Wake Forest University, School of Medicine, Winston-Salem, North Carolina 27157, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / physiology*
Axons / physiology*,  ultrastructure
Caspases / antagonists & inhibitors
Cell Division / physiology
Chick Embryo
Cysteine Proteinase Inhibitors / pharmacology
N-Methylaspartate / pharmacology
Neuregulin-1 / metabolism*
Neuregulins / metabolism
Oculomotor Nerve / cytology,  drug effects,  embryology
Peripheral Nerves / cytology,  drug effects,  embryology
Receptor, Nerve Growth Factor / metabolism
Receptors, Platelet-Derived Growth Factor / metabolism
Schwann Cells / cytology*,  drug effects,  ultrastructure
Signal Transduction
Spinal Nerve Roots / cytology,  drug effects,  embryology
Up-Regulation / physiology
Grant Support
ID/Acronym/Agency:
NS 36945/NS/NINDS NIH HHS; NS20402/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Cysteine Proteinase Inhibitors; 0/Neuregulin-1; 0/Neuregulins; 0/Receptor, Nerve Growth Factor; 6384-92-5/N-Methylaspartate; EC 2.7.10.1/Receptors, Platelet-Derived Growth Factor; EC 3.4.22.-/Caspases

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