Up-regulation of the Ang II/AT1 receptor may compensate for the loss of gastric antrum ICC via the PI3k/Akt signaling pathway in STZ-induced diabetic mice
Up-regulation of the Ang II/AT1 receptor may compensate for the loss of gastric antrum ICC via the PI3k/Akt signaling pathway in STZ-induced diabetic mice
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STZ 诱导的糖尿病小鼠中 Ang II/AT1 受体的上调可能通过 PI3k/Akt 信号通路补偿胃窦 ICC 的损失
DOI：
10.1016/j.mce.2016.01.002
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发表时间：
2016-03
影响因子：
4.1
通讯作者：
Xu, W. X.
中科院分区：
文献类型：
--
作者：
Meng, X. M.;Liu, D. H.;Kim, Young-chul;Xu, W. X.
The classic renin–angiotensin system (RAS) is a complex system in which angiotensin II (Ang II) has been identified as an important endogenous regulator that influences both smooth muscle contraction and cell growth. Although a local RAS is known to exist in the gastrointestinal tract, it is unclear whether Ang II is involved in the loss of gastric interstitial cells of Cajal (ICC) in diabetic mice. The present study was designed to investigate the effect of Ang II on ICC survival in streptozotocin (STZ)-induced diabetic mice. Western blot, immunofluorescence, isometric muscle recording, enzyme-linked immunosorbent assay (ELISA) and a cell counting kit-8 were used in this research. Our results demonstrate that the c-Kit and membrane-bound stem cell factor (mSCF) protein expression levels in gastric smooth muscle were decreased in STZ-induced diabetic mice. However, the angiotensin receptor type 1 (AT1R) expression levels in gastric smooth muscle and angiotensin-converting enzyme (ACE) expression levels in gastric mucosa were increased. The effect of Ang II on the tonic contraction of gastric smooth muscle was potentiated in diabetic mice, and the plasma Ang II level was enhanced. Ang II increased mSCF expression, cell proliferation, and Akt-Ser473 phosphorylation in cultured gastric smooth muscle cells (GSMCs). These effects were reduced by specific inhibitors ZD7155 (an AT1R antagonist) and LY294002 (a PI3-kinase inhibitor). Our results suggest that Ang II increases mSCF expression and cell proliferation in cultured GSMCs in a PI3K/Akt signaling-dependent manner. ACE and AT1R up-regulation in the stomach may help compensate for ICC loss in STZ-induced diabetic mice.
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影响因子：
21.1
作者：
R. Touyz;E. Schiffrin
通讯作者：
R. Touyz;E. Schiffrin
DOI：
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发表时间：
2006
期刊：
--
影响因子：
--
作者：
H. Ohtsu;Hiroyuki Suzuki;H. Nakashima;Sudhir Dhobale;G. D. Frank;E. Motley;S. Eguchi
通讯作者：
H. Ohtsu;Hiroyuki Suzuki;H. Nakashima;Sudhir Dhobale;G. D. Frank;E. Motley;S. Eguchi
影响因子：
29.4
作者：
Parkman HP;Yates K;Hasler WL;Nguyen L;Pasricha PJ;Snape WJ;Farrugia G;Koch KL;Abell TL;McCallum RW;Lee L;Unalp-Arida A;Tonascia J;Hamilton F;National Institute of Diabetes and Digestive and Kidney Diseases Gastroparesis Clinical Research Consortium
通讯作者：
National Institute of Diabetes and Digestive and Kidney Diseases Gastroparesis Clinical Research Consortium
影响因子：
5.6
作者：
Zhao, Yanbin;Chen, Xuesong;Fu, Songbin
通讯作者：
Fu, Songbin
血管紧张素 II 上调人血管内皮细胞和平滑肌细胞中胎盘生长因子的表达。
影响因子：
--
作者：
Pan P;Fu H;Zhang L;Huang H;Luo F;Wu W;Guo Y;Liu X
通讯作者：
Liu X