Knockdown of ASIC2a subunit aggravates injury of rat C6 glioma cells in acidosis |
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Authors: | Xiao-Yan Liu Shu-Zhuo Zhang Xiao-Yun Ma Hui Wang Bao-Hong Wu Hong-Liang Sun Xin Li Xiao-Li Wei Jian-Quan Zheng |
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Institution: | (1) Department of Biochemical Pharmacology, Beijing Institute of Pharmacology and Toxicology, 27 Taiping Rd, Beijing, 100850, China; |
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Abstract: | Acid-sensing ion channel 1a (ASIC1a) and 2a (ASIC2a) subunits are widely expressed throughout mammalian central nervous system.
Activation of Ca2+-permeable ASIC1a homomultimers is largely responsible for acidosis-mediated, glutamate receptor-independent, ischemic neuronal
injury. The function of ASIC2a in brain ischemia is less known except that transient global ischemia induces ASIC2a protein
expression up-regulation in neurons that survived ischemia. Acidosis is assumed to play a critical role in brain ischemia
injury. In the present experiment, rat C6 neuroglioma cells were used to explore the function of ASIC2a. MTT and relative
LDH release assay revealed that knockdown of ASIC2a could aggravate the acidosis-induced injury of C6 cells. Through changing
extracellular Ca2+ concentration and measuring intracellular calcium fluorescence intensity, it was found that aggravated damage was due to
toxic Ca2+ overload via ASICs mechanisms. The current results indicated that, different from ASIC1a, ASIC2a probably played a protective
role against the injury induced by extracellular acidosis in C6 cells. |
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