Peng Dong1, Minglong Liu2, Chaofeng Liu3. 1. Department of Endocrinology. 2. Intensive Care Unit, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an 710004. 3. Department of Cardiology, Shaanxi Provincial Hospital of Traditional Chinese Medicine, 710021, China.
Abstract
BACKGROUND: KCa3.1 ion channels play an important role during atherosclerosis. We aimed to investigate the effect of exenatide on KCa3.1 expression in aortic vascular smooth muscle cells (VSMCs) of diabetic rats. METHODS: Sprague-Dawley rats were randomly divided into normal control (NC), diabetes model (DM), and exenatide treatment (ET) groups. Hematoxylin and eosin and α-actin immunohistochemical staining were used to detect changes in rat aortic vascular smooth muscle. Quantitative RT-PCR and Western blot analysis were used to detect changes in KCa3.1 mRNA and protein levels, respectively. RESULTS: Aortic tissue staining in the DM group revealed an absence of smooth or integrated endothelium, increased smooth muscle cell proliferation in the media, smooth muscle hyperplasia, disorganized smooth muscle cells, and an increased number of collagen fibers, relative to the NC and ET groups. KCa3.1 mRNA expression was higher in the DM group than in the NC and ET groups. Similarly, the KCa3.1 protein level was higher in the DM group than in the NC and ET groups. The KCa3.1 protein level did not significantly differ between the ET and NC groups. CONCLUSIONS: Exenatide could inhibit the expression of the KCa3.1 channel in VSMCs of diabetic rats.
BACKGROUND: KCa3.1 ion channels play an important role during atherosclerosis. We aimed to investigate the effect of exenatide on KCa3.1 expression in aortic vascular smooth muscle cells (VSMCs) of diabetic rats. METHODS: Sprague-Dawley rats were randomly divided into normal control (NC), diabetes model (DM), and exenatide treatment (ET) groups. Hematoxylin and eosin and α-actin immunohistochemical staining were used to detect changes in rat aortic vascular smooth muscle. Quantitative RT-PCR and Western blot analysis were used to detect changes in KCa3.1 mRNA and protein levels, respectively. RESULTS: Aortic tissue staining in the DM group revealed an absence of smooth or integrated endothelium, increased smooth muscle cell proliferation in the media, smooth muscle hyperplasia, disorganized smooth muscle cells, and an increased number of collagen fibers, relative to the NC and ET groups. KCa3.1 mRNA expression was higher in the DM group than in the NC and ET groups. Similarly, the KCa3.1 protein level was higher in the DM group than in the NC and ET groups. The KCa3.1 protein level did not significantly differ between the ET and NC groups. CONCLUSIONS: Exenatide could inhibit the expression of the KCa3.1 channel in VSMCs of diabetic rats.
Entities:
Keywords:
Atherosclerosis; Ion channel; Vascular smooth muscle cells
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