Research on Potential Role of Receptor-interacting Protein Kinase1 in Phenotype Switching of Vascular Smooth Muscle Cells_Journal of Biomedical Engineering

Authors：

1. Department of Cardiology, West China Hospital, Sichuan University, Chengdu 610041, China;
2. Laboratory of Cardiovascular Diseases, Regenerative Medicine Research Center, West China Hospital, Sichuan University, Chengdu 610041, China;

Corresponding author：

Keywords：

receptor-interacting protein kinases 1; vascular smooth muscle cells phenotypic switching; Angiotensin Ⅱ; nuclear transcription fator-κB

DOI：

10.7507/1001-5515.20160118

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Vascular smooth muscle cells (VSMCs) phenotype switching plays an essential role in the pathogenesis of various vascular diseases. The present study aims to investigate the role of receptor-interacting protein kinases 1(RIPK1) in VSMCs phenotypic switching induced by Angiotensin Ⅱ(Ang Ⅱ). Expression of mRNA and protein of RIPK1, markers of VSMCs phenotypic switching and secretion, phosphorylation of the P65 subunit of NF-κB were measured by real-time PCR and Western blot. Meanwhile, EdU incorporation assay and wound scratch assay were performed to determine the cell proliferation and migration respectively. At the same time, Necrostatin-1(Nec-1, an known RIPK1 inhibitor) and RIPK1-specific small interference RNA (siRNA) were used to inhibit the expression of RIPK1. The experimental data demonstrated that the mRNA and protein levels of RIPK1 and P65 phosphorylation were increased significantly in the process of VSMC phenotypic switching induced by Ang II. Moreover, the expression of RIPK1 and P65 phosphorylation were significantly down-regulated in VSMCs pretreated with Nec-1 or trans-fected with RIPK1-siRNA. Furthermore, the proliferation, secretion and migration of VSMCs were also markedly suppressed after inhibition of RIPK1 by Nec-1 or its specific siRNA. The results suggested that RIPK1 might be involved in VSMC phenotypic switching induced by Ang II, which was possibly via up-regulating the NF-κB signaling pathway.

Citation： BAOQinxue, CHENLi, WUSiyuan, ZHAOMingyue, WUWenchao, FUHua, LIUXiaojing. Research on Potential Role of Receptor-interacting Protein Kinase1 in Phenotype Switching of Vascular Smooth Muscle Cells. Journal of Biomedical Engineering, 2016, 33(4): 719-728. doi: 10.7507/1001-5515.20160118 Copy

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22.	NEWTON K. RIPK1 and RIPK3:critical regulators of inflammation and cell death[J]. Nat Immunol, 2015, 25(6):347-353.
23.	FEOKTISTOVA M, LEVERKUS M. Programmed necrosis and necroptosis signalling[J]. FEBS J, 2015, 282(1):19-31.
24.	DENG Bin, FANG Fang, YANG Tianlu, et al. Ghrelin inhibits AngⅡ-induced expression of TNF-alpha, IL-8, MCP-1 in human umbilical vein endothelial cells[J]. Int J Clin Exp Med, 2015, 8(1):579-588.
25.	SILKE J, RICKARD J A, GERLIC M. The diverse role of RIP kinases in necroptosis and inflammation[J]. Nat Immunol, 2015, 16(7):689-697.
26.	FREISE C, KIM K Y, QUERFELD U. A lindera obtusiloba extract blocks calcium-/Phosphate-Induced transdifferentiation and calcification of vascular smooth muscle cells and interferes with matrix metalloproteinase-2 and metalloproteinase-9 and NF-kappaB[J]. Evid Based Complement Alternat Med, 2015:679238.

1. HU Qi, CHEN Jing, ZHANG Jing, et al. IOX1, a JMJD2A inhibitor, suppresses the proliferation and migration of vascular smooth muscle cells induced by angiotensin Ⅱ by regulating the expression of cell cycle-related proteins[J]. Int J Mol Med, 2016, 37(1):189-196.
2. DAVIS D N. WU C, HATA A.micromanaging vascular smooth muscle cell differentiation and phenotypic modulation[J]. Arterioscler Thromb Vasc Biol, 2011, 31(11):2370-2377.
3. SPIN J M, MAEGDEFESSEL L, TSAO P S. Vascular smooth muscle cell phenotypic plasticity:focus on chromatin remodelling[J]. Cardiovasc Res, 2012, 95(2):147-155.
4. LAN Taohua, HUANG Xiongqing, TAN Hongmei. Vascular fibrosis in atherosclerosis[J]. Cardiovasc Pathol, 2013, 22(5):401-407.
5. SHANKMAN L S, GOMEZ D, CHEREPANOVA O A, et al. KLF4-dependent phenotypic modulation of smooth muscle cells has a key role in atherosclerotic plaque pathogenesis[J]. Nat Med, 2015, 21(6):628-637.
6. GOMEZ D, OWENS G K. Smooth muscle cell phenotypic switching in atherosclerosis[J]. Cardiovasc Res, 2012, 95(2):156-164.
7. MORROW D, GUHA S, SWEENEY C, et al. Notch and vascular smooth muscle cell phenotype[J]. Circ Res, 2008, 103(12):1370-1382.
8. YOSHIDA T, YAMASHITA M, HORIMAI C, et al. Smooth Muscle-Selective inhibition of nuclear factor-kappa B attenuates smooth muscle phenotypic switching and neointima formation following vascular injury[J]. J Am Heart Assoc, 2013, 2(3):e000230.
9. LEE K Y, LEE D H, CHOI H C. C.mesoglycan attenuates VSMC proliferation through activation of AMP-activated protein kinase and mTOR[J]. Clin Hypertens, 2015, 22:2.
10. WEINLICH R, GREEN D R. The two faces of receptor interacting protein kinase-1[J]. Mol Cell, 2014, 56(4):469-480.
11. ZHAO Mingyue, LU Lihui, LEI Song, et al. Inhibition of receptor interacting protein kinases attenuates cardiomyocyte hypertrophy induced by palmitic acid[J]. Oxid Med Cell Longev, 2016:1451676.
12. TAKAHASHI N, VEREECKE L, BERTRAND M J, et al. RIPK1 ensures intestinal homeostasis by protecting the epithelium against apoptosis[J]. Nature, 2014, 513(7516):95-99.
13. DOHRMAN A, KATAOKA T, CUENIN S, et al. Cellular FLIP(long form)regulates CD8+T cell activation through caspase-8-dependent NF-kappa B activation[J]. J Immunol, 2005, 174(9):5270-5278.
14. OERLEMANS M I, LIU J, ARSLAN F, et al. Inhibition of RIP1-dependent necrosis prevents adverse cardiac remodeling after myocardial ischemia-reperfusion in vivo[J]. Basic Res Cardiol, 2012, 107(4):270.
15. LI Yang, TAO Jie, ZHANG Jian, et al. Cellular repressor E1A-stimulated genes controls phenotypic switching of adventitial fibroblasts by blocking p38MAPK activation[J]. Atherosclerosis, 2012, 225(2):304-314.
16. HE Q, MAN L, JI Y, et al. Comparison in the biological characteristics between primary cultured sensory and motor Schwann cells[J]. Neurosci Lett, 2012, 521(1):57-61.
17. 牛珩, 张金国.黄芪甲苷对肿瘤坏死因子诱导的大鼠血管平滑肌细胞增殖迁移的影响[J].临床心血管病杂志, 2015, 31(10):1111-1115.
18. 陆立慧, 赵明月, 吴思媛, 等.抑制程序性坏死对缺氧/复氧H9c2心肌细胞损伤的影响[J].生物医学工程学杂志, 2015, 32(2):393-399.
19. LU H, DAUGHERTY A. Atherosclerosis[J]. Arterioscler Thromb Vasc Biol, 2015, 35(3):485-491.
20. ZHANG Y N, XIE B D, SUN L, et al. Phenotypic switching of vascular smooth muscle cells in the 'normal region' of aorta from atherosclerosis patients is regulated by miR-145[J]. J Cell Mol Med, 2016:1-13.
21. PAUDEL K R, KARKI R, KIM D W. Cepharanthine inhibits in vitro VSMC proliferation and migration and vascular inflammatory responses mediated by RAW264.7[J]. Toxicol In Vitro, 2016, 34:16-25.
22. NEWTON K. RIPK1 and RIPK3:critical regulators of inflammation and cell death[J]. Nat Immunol, 2015, 25(6):347-353.
23. FEOKTISTOVA M, LEVERKUS M. Programmed necrosis and necroptosis signalling[J]. FEBS J, 2015, 282(1):19-31.
24. DENG Bin, FANG Fang, YANG Tianlu, et al. Ghrelin inhibits AngⅡ-induced expression of TNF-alpha, IL-8, MCP-1 in human umbilical vein endothelial cells[J]. Int J Clin Exp Med, 2015, 8(1):579-588.
25. SILKE J, RICKARD J A, GERLIC M. The diverse role of RIP kinases in necroptosis and inflammation[J]. Nat Immunol, 2015, 16(7):689-697.
26. FREISE C, KIM K Y, QUERFELD U. A lindera obtusiloba extract blocks calcium-/Phosphate-Induced transdifferentiation and calcification of vascular smooth muscle cells and interferes with matrix metalloproteinase-2 and metalloproteinase-9 and NF-kappaB[J]. Evid Based Complement Alternat Med, 2015:679238.

Journal of Biomedical Engineering

Research on Potential Role of Receptor-interacting Protein Kinase1 in Phenotype Switching of Vascular Smooth Muscle Cells

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