中国作者重要发表 - BMP6通过Smad蛋白依赖的HO-1诱导抑制HK



BMP6通过Smad蛋白依赖的HO-1诱导抑制HK - 2细胞的氧化损伤





BMP6 attenuates oxidant injury in HK-2 cells via Smad-dependent HO-1 induction





Yan J., Yang S., Zhang J., Zhai C., Zhu T. 2009/5/29 18:38:57

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Free Radical Biology and Medicine, 2009, Volume 46, Issue 9




Oxidative stress is involved in a variety of kidney diseases, and heme oxygenase 1 (HO-1) induction is a protective response to oxidative stress. Downregulation of bone morphogenetic protein 6 (BMP6) is associated with renal damage in intrauterine growth-restricted newborns. However, it is unknown whether BMP6 has a renoprotective effect or HO-1 induction property. In this study, we demonstrate that BMP6 effectively protects renal proximal tubule cells (HK-2) against hydrogen peroxide (H2O2)-induced cell injury. BMP6 also increased HO-1 gene expression and activity of HO. Inhibition of de novo gene expression, the HO inhibitor ZnPPIX, HO-1 knockdown, or the carbon monoxide (CO) scavenger hemoglobin attenuated the cytoprotective effect of BMP6, whereas HO-1 constitutive expression, the HO-1 inducer hemin, or the hemin metabolites bilirubin and CO ameliorated H2O2-induced cell injury. Stimulation of HK-2 cells with BMP6 activated Smad signaling but not mitogen-activated protein kinases. In addition, BMP6-mediated induction of HO-1 expression and increase in HO activity were inhibited by Smad5 knockdown. Furthermore, deletion or mutation of the Smad-binding element in the HO-1 promoter also inhibited BMP6-induced luciferase activity. In summary, these findings suggest that induction of HO-1 through a Smad-dependent mechanism is responsible for the cytoprotective effect of BMP6 in H2O2-mediated renal cell injury. © 2009 Elsevier Inc. All rights reserved.



Correspondence Address: Zhu, T.; Medical College, Nankai University, Tianjin, 300071, China; email: zhuth@nankai.edu.cn



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