Xiong Jing, Wang Yang, Zhu Zhonghua, Liu Jianshe, Wang Yumei, Zhang Chun, Hammes Hans-Peter, Lang Florian, Feng Yuxi
Department of Nephrology, Union Hospital, Tongji Medical College, Huangzhong University of Science & Technology, Wuhan, China.
Biochem Biophys Res Commun. 2007 Oct 5;361(4):960-7. doi: 10.1016/j.bbrc.2007.07.113. Epub 2007 Jul 30.
As a membrane-spanning protein, NG2 chondroitin sulfate proteoglycan interacts with molecules on both sides of plasma membrane. The present study explored the role of NG2 in the pathogenesis of diabetic nephropathy. In the normal kidneys, NG2 was observed predominantly in glomerular mesangium, Bowman's capsule and interstitial vessels. Both mRNA and protein expression in kidneys was significantly higher in strepozotocin-induced diabetic rats than that in normal rats. In the cultured rat mesangial cell line HBZY-1, overexpression of NG2 promoted mesangial cell proliferation and extracellular matrix (ECM) production, such as type VI collagen and laminin. Furthermore, target knockdown of NG2 resulted in decreased cell proliferation and ECM formation. The observations suggest that NG2 is up-regulated in diabetic nephropathy. It actively participates in the development and progression of glomerulosclerosis by stimulating proliferation of mesangial cells and deposition of ECM.
作为一种跨膜蛋白,NG2硫酸软骨素蛋白聚糖与质膜两侧的分子相互作用。本研究探讨了NG2在糖尿病肾病发病机制中的作用。在正常肾脏中,NG2主要在肾小球系膜、鲍曼囊和间质血管中观察到。链脲佐菌素诱导的糖尿病大鼠肾脏中的mRNA和蛋白表达均显著高于正常大鼠。在培养的大鼠系膜细胞系HBZY-1中,NG2的过表达促进了系膜细胞增殖和细胞外基质(ECM)产生,如VI型胶原和层粘连蛋白。此外,NG2的靶向敲低导致细胞增殖和ECM形成减少。这些观察结果表明,NG2在糖尿病肾病中上调。它通过刺激系膜细胞增殖和ECM沉积,积极参与肾小球硬化的发生和发展。