T-2 toxin exposure induces apoptosis in tm3 cells by inhibiting mammalian target of rapamycin/serine/threonine protein kinase(Mtorc2/akt) to promote ca2+ production
National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [31302157]; China Postdoctoral Science FoundationChina Postdoctoral Science Foundation [2017M620346]; Scientific Research Project of Hunan Provincial Education Department [17B125]
机构署名：
本校为第一且通讯机构
院系归属：
动物医学院
摘要：
Although mTOR (the mammalian target of rapamycin) can regulate intracellular free Ca2+concentration in normal cultured podocytes, it remains elusive as to how mTORC2/AKT-mediated Ca2+participates in the process of T-2 toxin-induced apoptosis. The potential signaling responsible for intracellular Ca2+ concentration changes was investigated using immunoblot assays in an in vitro model of TM3 cell injury induced by T-2 toxin. Changes in Ca2+ were assessed using the Ca2+-sensitive fluorescent indictor dye Fura 2-AM. The cytotoxicity of TM3 cells was assessed with an MTT bioassay, and apoptosis was...
