【摘 要】
：
Ca2+ leak induces the mitochondria or sarco/endoplasmic reticulum (SR/ER)related cell death.In the present study ,we examined the contribution of SR-released Ca2+ through ryanodine receptors (RyR)to t
【机 构】
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Department of Veterinary Medicine, Northeast Agricultural University, Harbin 150030,P.R.China
【出 处】
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中国畜牧兽医学会兽医内科与临床诊疗学分会第八届代表大会暨学术研讨会
论文部分内容阅读
Ca2+ leak induces the mitochondria or sarco/endoplasmic reticulum (SR/ER)related cell death.In the present study ,we examined the contribution of SR-released Ca2+ through ryanodine receptors (RyR)to the muscular injuries in Selenoprotein W (Selw) silencing myoblast model.The results showed that Selw deficiency induced Ca2+ release from SR,which led the accumulation of Ca2+ in mitochondria as well as higher production of ROS and the damaged ultrastructure of mitochondria and SR.In addition,Selw silencing elevated the levels of ATF4, ATF6,IRE1, GRP78, GRP94, eIF2α, CytC as well as the activation of CHOP, Caspase9, and Caspase3.By detecting the S-glutathionylation of RyR1 and Ca2+ signal,we found that oxidation-RyR1-induced Ca2+ leak regulated ER stress,mitochondria-SR related cell apoptosis in Selw deficiency myoblast.The present study showed that mitochondria-SR related cell death was involved in Selw induced muscular injuries.For the first time,we found that Selw induced Ca2+ leak,ER stress,and ER related apoptosis in myoblast.In addition,oxidation-RyR1-induced Ca2+ leak played important role in regulating mitochondria-SR related crosstalk in Selw deficiency myoblast.
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