The effects of Interleukin-20 on vascular smooth muscle cells

• Main Authors: Lu-fei Chen, 陳入妃
• Other Authors: Ming-shi Chang
• Format: Others
• Language: zh-TW
• Published: 2008
• Online Access: http://ndltd.ncl.edu.tw/handle/72338566917346453934

碩士 === 國立成功大學 === 生物化學研究所 === 96 === Hypertension is characterized by the remodeling of arterial wall. This remodeling involves changes in arterial wall components leading to arterial stiffness, which is induced by inflammation, endothelium dysfunction and hypertrophy of vascular smooth muscle cells (VSMCs). All promote vasoconstriction and create a situation ripe for establishment of atherosclerotic plaques. Interleukin-20 (IL-20) belongs to IL-10 family and is a proinflammatory cytokine. Previous studies showed that IL-20 has both direct and indirect angiogenic effects on endothelial cells to promote the progression of atherosclerosis. In this study, we found that IL-20 in the serum of spontaneous hypertension rat (SHR) is higher than that of healthy control (WKY). Therefore, we were aimed to explore the roles of IL-20 in VSMCs involved in the pathogenesis of hypertension. We analyzed the expression of IL-20 and its receptor complex, IL-20R1/R2 and IL-20R2/IL-22R1, in VSMCs isolated from spontaneous hypertension rats (SHR) and control rats (Wistar Kyoto, WKY) by using RT-PCR. Then, we performed MTT assay, ROS assay and migration assay to examine the effects of IL-20 on VSMCs. Our results showed that both VSMCs could be the target cells of IL-20 due to the expression of its receptors on these cells. IL-20 had no significant effect on proliferation and ROS production in VSMCs. However, IL-20 induced the migration of SHR VSMCs through ERK1/2 and STAT-3 pathway. Moreover, in response to IL-20, SHR VSMCs produced TNF-α and IL-1���z�ntwo important risk factors involved in hypertension. In addition, IL-20 induced cell migration of SHR VSMCs through up-regulation of IGF and down-regulation of E-cadherin. Taken together, IL-20 may be involved in enhancing migration of vascular smooth muscle cells and inducing inflammatory response in spontaneous hypertension rat model.