Li X, Jiang L, Yang M, Wu Y, Sun S, Sun J
Department of Endocrinology, Zhongnan Hospital, Wuhan University, Wuhan, 430071, China.
Department of Internal Medicine, Zhongnan Hospital, Wuhan University, Wuhan, 430071, China.
J Endocrinol Invest. 2015 Jan;38(1):73-9. doi: 10.1007/s40618-014-0156-8. Epub 2014 Aug 23.
To investigate the effects of Exendin-4 (Ex-4), a glucagon-like peptide-1 (GLP-1) receptor agonist, on the expression of C1q/TNF-related protein-3 (CTRP3), a novel adipokine, in 3T3-L1 adipocytes. The role of protein kinase A (PKA) signal pathway in the effects was also investigated.
The mRNA and protein expressions of CTRP3 in 3T3-L1 adiocytes were detected by real-time polymerase chain reaction and western blot, respectively. Exendin-fragment 9-39 (Ex-9), a specific GLP-1 receptor antagonist, and H89, a selective antagonist of PKA, were used to confirm the signal pathway of Ex-4 on CTRP3.
2.5 or 5.0 nmol/l Ex-4 treatment for 8 h increased the expressions of CTRP3 mRNA and protein as well as PKA protein in 3T3-L1 adipocytes significantly, while Ex-9 or H89 blocked the up-regulation of CTRP3 expression induced by Ex-4 completely.
GLP-1 receptor agonist increases the expression of CTRP3 mRNA and protein in 3T3-L1 adipocytes via PKA signal pathway.
研究胰高血糖素样肽-1(GLP-1)受体激动剂艾塞那肽-4(Ex-4)对3T3-L1脂肪细胞中新型脂肪因子C1q/TNF相关蛋白-3(CTRP3)表达的影响。同时研究蛋白激酶A(PKA)信号通路在该效应中的作用。
分别采用实时聚合酶链反应和蛋白质印迹法检测3T3-L1脂肪细胞中CTRP3的mRNA和蛋白表达。使用GLP-1受体特异性拮抗剂艾塞那肽片段9-39(Ex-9)和PKA选择性拮抗剂H89来确定Ex-4对CTRP3的信号通路。
2.5或5.0 nmol/l Ex-4处理8小时可显著增加3T3-L1脂肪细胞中CTRP3 mRNA和蛋白以及PKA蛋白的表达,而Ex-9或H89可完全阻断Ex-4诱导的CTRP3表达上调。
GLP-1受体激动剂通过PKA信号通路增加3T3-L1脂肪细胞中CTRP3 mRNA和蛋白的表达。