TRB3 is involved in free fatty acid-induced INS-1-derived cell apoptosis via the protein kinase C δ pathway.
TRB3 is involved in free fatty acid-induced INS-1-derived cell apoptosis via the protein kinase C δ pathway.
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TRB3 通过蛋白激酶 C δ 途径参与游离脂肪酸诱导的 INS-1 衍生细胞凋亡
DOI：
10.1371/journal.pone.0096089
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Chen L
中科院分区：
文献类型：
--
作者：
Qin J;Fang N;Lou J;Zhang W;Xu S;Liu H;Fang Q;Wang Z;Liu J;Men X;Peng L;Chen L
Chronic exposure to free fatty acids (FFAs) may induce β cell apoptosis in type 2 diabetes. However, the precise mechanism by which FFAs trigger β cell apoptosis is still unclear. Tribbles homolog 3 (TRB3) is a pseudokinase inhibiting Akt, a key mediator of insulin signaling, and contributes to insulin resistance in insulin target tissues. This paper outlined the role of TRB3 in FFAs-induced INS-1 β cell apoptosis. TRB3 was promptly induced in INS-1 cells after stimulation by FFAs, and this was accompanied by enhanced INS-1 cell apoptosis. The overexpression of TRB3 led to exacerbated apoptosis triggered by FFAs in INS-1-derived cell line and the subrenal capsular transplantation animal model. In contrast, cell apoptosis induced by FFAs was attenuated when TRB3 was knocked down. Moreover, we observed that activation and nuclear accumulation of protein kinase C (PKC) δ was enhanced by upregulation of TRB3. Preventing PKCδ nuclear translocation and PKCδ selective antagonist both significantly lessened the pro-apoptotic effect. These findings suggest that TRB3 was involved in lipoapoptosis of INS-1 β cell, and thus could be an attractive pharmacological target in the prevention and treatment of T2DM.
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影响因子：
3.5
作者：
Cheng, Qun;Dong, Weipin;Peng, Yongde
通讯作者：
Peng, Yongde
影响因子：
7.7
作者：
Carpenter, L;Cordery, D;Biden, TJ
通讯作者：
Biden, TJ
影响因子：
4.8
作者：
Humphrey, Rohan K.;Newcomb, Christina J.;Jhala, Ulupi S.
通讯作者：
Jhala, Ulupi S.
影响因子：
7.7
作者：
Cnop, M;Hannaert, JC;Pipeleers, DG
通讯作者：
Pipeleers, DG
影响因子：
4.8
作者：
Carpenter, L;Cordery, D;Biden, TJ
通讯作者：
Biden, TJ