Literature DB >> 16248974

Apoptotic cell death following traumatic injury to the central nervous system.

Joe E Springer1.   

Abstract

Apoptotic cell death is a fundamental and highly regulated biological process in which a cell is instructed to actively participate in its own demise. This process of cellular suicide is activated by developmental and environmental cues and normally plays an essential role in eliminating superfluous, damaged, and senescent cells of many tissue types. In recent years, a number of experimental studies have provided evidence of widespread neuronal and glial apoptosis following injury to the central nervous system (CNS). These studies indicate that injury-induced apoptosis can be detected from hours to days following injury and may contribute to neurological dysfunction. Given these findings, understanding the biochemical signaling events controlling apoptosis is a first step towards developing therapeutic agents that target this cell death process. This review will focus on molecular cell death pathways that are responsible for generating the apoptotic phenotype. It will also summarize what is currently known about the apoptotic signals that are activated in the injured CNS, and what potential strategies might be pursued to reduce this cell death process as a means to promote functional recovery.

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Year:  2002        PMID: 16248974     DOI: 10.5483/bmbrep.2002.35.1.094

Source DB:  PubMed          Journal:  J Biochem Mol Biol        ISSN: 1225-8687


  27 in total

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Journal:  Int J Exp Pathol       Date:  2010-10-05       Impact factor: 1.925

2.  Proteomic and phosphoproteomic analyses of the soluble fraction following acute spinal cord contusion in rats.

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5.  Effect of endogenous androgens on 17beta-estradiol-mediated protection after spinal cord injury in male rats.

Authors:  Supatra Kachadroka; Alicia M Hall; Tracy L Niedzielko; Sukumal Chongthammakun; Candace L Floyd
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6.  Experimental reovirus-induced acute flaccid paralysis and spinal motor neuron cell death.

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7.  Spatiotemporal pattern of RNA-binding motif protein 3 expression after spinal cord injury in rats.

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Journal:  Cell Mol Neurobiol       Date:  2014-02-26       Impact factor: 5.046

8.  Estrogen-like neuroprotection of isopsoralen against spinal cord injury through estrogen receptor ERα.

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9.  VGF (TLQP-62)-induced neurogenesis targets early phase neural progenitor cells in the adult hippocampus and requires glutamate and BDNF signaling.

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Journal:  Stem Cell Res       Date:  2014-03-26       Impact factor: 2.020

10.  Ovarian steroids decrease DNA fragmentation in the serotonin neurons of non-injured rhesus macaques.

Authors:  F B Lima; C L Bethea
Journal:  Mol Psychiatry       Date:  2009-10-13       Impact factor: 15.992

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