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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2010-3-1
pubmed:abstractText
Insulin-like growth factor-1 (IGF-1) is a neurotrophic factor and a potent anti-apoptotic factor. IGF-1 plays an important role in promoting axonal growth from dorsal root ganglion (DRG) neurons and prevents apoptosis in DRG neurons. Whether IGF-1 could modulate Ca2+ homeostasis and apoptosis of sensory DRG neurons with excitotoxicity induced by glutamate (Glu) is still unknown. In the present study, primary cultured DRG neurons were used to determine the effects of IGF-1 on Ca2+ homeostasis and apoptosis of sensory DRG neurons with excitotoxicity induced by Glu. Intracellular Ca2+ concentration ([Ca2+]i) in isolated DRG neurons using the fluorescent Ca2+ indicator fura-3 was measured by confocal laser scanning microscope (CLSM). Procaspase-3 expression was detected by Western blot analysis. Application of 0.2 mmol/L Glu evoked an increase in [Ca2+]i, confirming the excitatory effect of Glu at this stage. The decrease of procaspase-3 expression levels after application of 0.2 mmol/L Glu suggested the apoptotic effects of Glu. These effects could be inhibited by the presence of IGF-1. In conclusion, we demonstrated that IGF-1 could modulate Ca2+ homeostasis and apoptosis of sensory DRG neurons with excitotoxicity induced by Glu. Both Ca2+ homeostasis and caspase-3 processing were implicated as the underlying neuroprotective mechanisms of IGF-1.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0031-7144
pubmed:author
pubmed:issnType
Print
pubmed:volume
65
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5-8
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Insulin-like growth factor-1 modulates Ca2+ homeostasis and apoptosis of cultured dorsal root ganglion neurons with excitotoxicity induced by glutamate.
pubmed:affiliation
Department of Anatomy, Shandong University School of Medicine, Jinan, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't