Inflammation of the vascular microenvironment modulates distinct types of vascular cells, and plays important roles in promoting atherosclerosis, stenosis/restenosis, and vascular-related diseases. Nik-related kinase (Nrk), a member of the Ste20-type kinase family, has been reported to be selectively expressed in embryonic skeletal muscle. However, whether Nrk is expressed in adult vascular smooth muscle, and if it influences intimal hyperplasia is unclear. Dr. Jun-Yang Liou from the Institute of Cellular and System Medicine and collaborators assessed the expression of Nrk in vascular smooth muscle cells (VSMCs) and investigated its potential roles in regulating vascular inflammation, and subsequently elucidated clinical associations involving Nrk in atherosclerotic patients
Dr. Liou and team reported treatment of mouse VSMCs with lipopolysaccharide (LPS) or platelet-derived growth factor significantly reduced Nrk expression. In addition, expression of Nrk was significantly reduced in regions of neointimal formation caused by guide-wire carotid artery injuries in mice, as well as in human atherosclerotic tissues, when compared to normal vessels. The team identified that expression of matrix metalloproteinases (MMP3, MMP8 and MMP12) and inflammatory cytokines/chemokines (CCL6, CCL8, CCL11, CXCL1, CXCL3, CXCL5 and CXCL9) were synergistically induced by Nrk siRNA in LPS-treated mouse VSMCs. Moreover, the team found that resveratrol significantly impaired LPS- and Nrk siRNA-induced expression of MMP3, CCL8, CCL11, CXCL3 and CXCL5. These results suggested that Nrk may play important roles in regulating pathological progression of atherosclerosis or neointimal- hyperplasia-related vascular diseases. The above findings have been published in Aging (2020 Apr 24;12(8):7511-7533).
Citation: Lu, YJ; Jan, YJ; Ko, BS; Liang, SM; Chen, L; Wu, CC; Chin, CH; Kuo, CC; Yet, SF; Liou, JY. Expression of Nik-related kinase in smooth muscle cells attenuates vascular inflammation and intimal hyperplasia. Aging (2020 Apr 24;12(8):7511-7533).