Knockdown of ASIC2a subunit aggravates injury of rat C6 glioma cells in acidosis

• Autores: 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
• Localización: Journal of physiology and biochemistry, ISSN-e 1877-8755, ISSN 1138-7548, Vol. 67, Nº. 2, 2011, págs. 275-281
• Idioma: inglés
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• Resumen

  • 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.