IR@PKUHSC  > 北京大学第一临床医学院  > 肾脏内科
学科主题临床医学
Connective tissue growth factor increases matrix metalloproteinase-2 and suppresses tissue inhibitor of matrix metalloproteinase-2 production by cultured renal interstitial fibroblasts
Yang, Min; Huang, Haichang; Li, Jingzi; Huang, Wen; Wang, Haiyan
刊名WOUND REPAIR AND REGENERATION
2007-11-01
DOI10.1111/j.1524-475X.2007.00284.x
15期:6页:817-824
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Cell Biology ; Dermatology ; Medicine, Research & Experimental ; Surgery
研究领域[WOS]Cell Biology ; Dermatology ; Research & Experimental Medicine ; Surgery
关键词[WOS]HUMAN MESANGIAL CELLS ; GENE-EXPRESSION ; MYOFIBROBLAST DIFFERENTIATION ; TUBULOINTERSTITIAL FIBROSIS ; DIABETIC-NEPHROPATHY ; GELATINASE-A ; FACTOR-BETA ; GLOMERULOSCLEROSIS ; COLLAGEN ; MMP-2
英文摘要

The involvement of gelatinase (matrix metalloproteinase-2 [MMP-2] and MMP-9) in the matrix remodeling and development of tubulointerstitial fibrosis has been studied recently, but relatively little is known about the regulators and the mechanisms controlling the activation and expression of gelatinase in renal fibroblasts. In these studies, the production and underlying signaling pathway for gelatinase by exogenous connective tissue growth factor (CTGF) treatment were investigated. Here, we show that CTGF acts as a potent promoter of the activation and expression of MMP-2, but not MMP-9 in normal rat kidney fibroblasts cell line (NRK-49F). We found that CTGF significantly increased the activity of MMP-2, as well as MMP-2 protein in conditioned medium and MMP-2 mRNA levels in cells. In studies to address the mechanisms involved in the regulation of MMP-2 activity, we found that the tissue inhibitor of matrix metalloproteinase-2 (TIMP-2), the inhibitor of MMP-2, decreased significantly when cells were treated with CTGF. Further studies showed that extracellular signal-regulated kinase (ERK) signaling is responsible for most of the CTGF-induced MMP-2 expression and TIMP-2 suppression. When NRK-49F fibroblasts were incubated with CTGF, activation of ERK1/2 signaling was observed. Suppression of ERK1/2 activation with nontoxic concentrations of PD98059, a specific inhibitor of ERK activation, was associated with a reduction of CTGF-stimulated MMP-2 activity and protein expression. In addition, the CTGF-mediated reduction of TIMP-2 activity and protein expression was prevented when ERK1/2 activation was inhibited by PD98059. These results provide evidence that CTGF augments activation of MMP-2 through an effect on MMP-2 protein expression and TIMP-2 suppression, and that these effects are dependent on the activation of the ERK1/2 pathway.

语种英语
WOS记录号WOS:000251029500139
引用统计
被引频次:19[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/66966
专题北京大学第一临床医学院_肾脏内科
北京大学第一临床医学院_介入血管外科
北京大学第一临床医学院_药剂科
作者单位Peking Univ First Hosp, Div Nephrol, Beijing, Peoples R China
推荐引用方式
GB/T 7714
Yang, Min,Huang, Haichang,Li, Jingzi,et al. Connective tissue growth factor increases matrix metalloproteinase-2 and suppresses tissue inhibitor of matrix metalloproteinase-2 production by cultured renal interstitial fibroblasts[J]. WOUND REPAIR AND REGENERATION,2007,15(6):817-824.
APA Yang, Min,Huang, Haichang,Li, Jingzi,Huang, Wen,&Wang, Haiyan.(2007).Connective tissue growth factor increases matrix metalloproteinase-2 and suppresses tissue inhibitor of matrix metalloproteinase-2 production by cultured renal interstitial fibroblasts.WOUND REPAIR AND REGENERATION,15(6),817-824.
MLA Yang, Min,et al."Connective tissue growth factor increases matrix metalloproteinase-2 and suppresses tissue inhibitor of matrix metalloproteinase-2 production by cultured renal interstitial fibroblasts".WOUND REPAIR AND REGENERATION 15.6(2007):817-824.
条目包含的文件
条目无相关文件。
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Yang, Min]的文章
[Huang, Haichang]的文章
[Li, Jingzi]的文章
百度学术
百度学术中相似的文章
[Yang, Min]的文章
[Huang, Haichang]的文章
[Li, Jingzi]的文章
必应学术
必应学术中相似的文章
[Yang, Min]的文章
[Huang, Haichang]的文章
[Li, Jingzi]的文章
相关权益政策
暂无数据
收藏/分享
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。