TY - JOUR
T1 - Glycine protection of PC-12 cells against injury by ATP-depletion
AU - Zhang, Kan
AU - Weinberg, Joel M.
AU - Venkatachalam, Manjeri A.
AU - Dong, Zheng
N1 - Funding Information:
We appreciate technical assistance of Jinzhao Wang and Yogendra Patel. Zheng Dong is a recipient of the Lyndon Baines Johnson Research Award from the American Heart Association, a Patricia W. Robinson Young Investigator of the National Kidney Foundation, and a Carl W. Gottschalk Research Scholar of the American Society of Nephrology. This work was supported in part by grants from the Texas Advanced Research Program (Z. D.), the American Heart Association (Z. D.), the American Society of Nephrology (Z. D.), National Kidney Foundation (Z. D.) and the National Institutes of Health (DK58831 to Z. D., DK37139 to M. A. V., DK34275 to J. M. W.).
PY - 2003/6/1
Y1 - 2003/6/1
N2 - A distinctive mechanism of cell injury during ATP depletion involves the loss of cellular glycine. The current study examined whether provision of glycine during ATP depletion can prevent injury in PC-12 cells, a cell line with neuronal property. In addition, we have examined the role played by glycine receptors in cytoprotective effects of the amino acid. It was shown that ATP depletion led to plasma membrane damage in PC-12 cells, which was ameliorated by 0.25-5mM glycine. Cytoprotective activity of glycine was shared by alanine, but not by glutamate or γ-aminobutyric acid (GABA). Of interest, strychnine, an antagonist of glycine receptor, was also protective. The results, while suggesting the involvement of glycine receptor in cytoprotection, indicate that chloride channel activity of the receptor is dispensable. Such a scenario is further supported by the observation that removal of extracellular chloride did not affect ATP depletion-induced cell injury or its prevention by glycine. In short, this study has provided the first evidence for glycine protection of cells with neuronal properties. Cytoprotection may involve the glycine receptor; however, it can be dissociated from its channel activity.
AB - A distinctive mechanism of cell injury during ATP depletion involves the loss of cellular glycine. The current study examined whether provision of glycine during ATP depletion can prevent injury in PC-12 cells, a cell line with neuronal property. In addition, we have examined the role played by glycine receptors in cytoprotective effects of the amino acid. It was shown that ATP depletion led to plasma membrane damage in PC-12 cells, which was ameliorated by 0.25-5mM glycine. Cytoprotective activity of glycine was shared by alanine, but not by glutamate or γ-aminobutyric acid (GABA). Of interest, strychnine, an antagonist of glycine receptor, was also protective. The results, while suggesting the involvement of glycine receptor in cytoprotection, indicate that chloride channel activity of the receptor is dispensable. Such a scenario is further supported by the observation that removal of extracellular chloride did not affect ATP depletion-induced cell injury or its prevention by glycine. In short, this study has provided the first evidence for glycine protection of cells with neuronal properties. Cytoprotection may involve the glycine receptor; however, it can be dissociated from its channel activity.
KW - ATP-depletion
KW - Cell injury
KW - Glycine
KW - Ischemia
KW - Neuron
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U2 - 10.1023/A:1023275426637
DO - 10.1023/A:1023275426637
M3 - Article
C2 - 12718443
AN - SCOPUS:0347155573
SN - 0364-3190
VL - 28
SP - 893
EP - 901
JO - Neurochemical Research
JF - Neurochemical Research
IS - 6
ER -