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SMAD3介导TGF-β1抑制MMP9在COS7细胞中的表达 被引量:4

TGF-β1 Mediated by SMAD3 Inhibits the Expression of MMP9 in COS7 Cells
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摘要 用明胶酶谱的方法检查了野生型和Smad3ex8 ex8纯合突变小鼠血清中基质金属蛋白酶(MMP9)的活性 .发现突变小鼠血清中MMP9的含量较正常小鼠的明显增高 ,提示SMAD3有抑制MMP9表达的功能 .通过细胞转染实验证实 ,TGF β1和野生型的SMAD3可以抑制COS7细胞分泌MMP9,而C端缺失的突变型Smad3基因过表达可以解除这种抑制作用 ,说明SMAD3介导TGF β1信号抑制MMP9在COS7细胞中的表达 . The amount of MMP9 in serum of wild type and Smad 3 ex8/ex8 homozygous mice was examined by gelatin zymography. The results showed that the amount of MMP9 in serum of mutant mice is higher than that of wild type mice. It suggested that SMAD3 could inhibit the expression of MMP9, which was verified by transient cell transfection experiments. The expression of MMP9 in COS7 cells decreased about 20% ( n=3, P <0.05) when treated with TGF β1 and almost stopped when transfected with wild type Smad 3 gene, suggesting that the expression of MMP9 could be inhibited by TGF β1 and the over expression of wild type Smad 3 gene. The expression of MMP9 in the samples transfected with C terminal truncated Smad 3 gene was similar to the control (n=3, P <0.05),indicating that the over expression of the C terminal truncated Smad 3 gene could block this inhibition. The data suggested that SMAD3 could mediate TGF β1 to inhibit the expression of MMP9 in COS7 cells.
出处 《中国生物化学与分子生物学报》 CAS CSCD 北大核心 2002年第6期684-687,共4页 Chinese Journal of Biochemistry and Molecular Biology
基金 国家自然科学基金项目 (No.3 9970 413 ) 国家杰出青年科学基金(No .3 0 0 2 5 0 2 8)资助
关键词 SMAD3 TGF-Β1 抑制 MMP9 COS7细胞 表达 MMP9, SMAD3, TGF β1, COS7
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  • 1Chang H,Development,1999年,126卷,8期,1631页
  • 2Yang X,Development,1999年,126卷,8期,1571页
  • 3Yang X,EMBO J,1999年,18卷,1280页
  • 4Datto M B,Mol Cell Biol,1999年,19卷,2495页
  • 5Shi Y,Cell,1998年,94卷,585页
  • 6Zhu Y,Cell,1998年,94卷,703页
  • 7Lo R S,EMBO J,1998年,17卷,996页
  • 8Feng X H,Genes Development,1998年,12卷,2153页
  • 9Hua X,Genes Development,1998年,12卷,3084页
  • 10Zawel L,Mol Cell,1998年,1卷,611页

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  • 1毛春明,杨晓,张莉,孙彦洵,侯宁,吕娅歆,黄翠芬.Smad3基因缺失加快的小鼠皮肤创面收缩速度机制研究[J].中国临床康复,2004,8(26):5538-5540. 被引量:6
  • 2Tardif G, Reboul P, Dupuls M, et al. Transforming growth factor-beta induced collagenase-3 production in human osteoarthritic chondrocytes is trigged by Smad proteins:cooperation between activator protein-1 and PEA-3 binding sites[J]. J Rheumatol, 2001,28
  • 3Mizui T, Ishimaru J, Miyamoto K, et al. Matrix metalloproteinase-2 in syn ovial lavage fluid of patients with disorders of the temporomandibular joint [J]. Br J Oral Maxillofac Surg, 2001,39:310
  • 4Woessner JF Jr, Gunja-Smith Z. Role of metalloproteinases in human osteoarthritis[J]. J Rheumatol Suppl, 1991,27:99
  • 5Nagase H, Woessner, JF Jr. Matrix metalloproteinases[J]. J Biol Chem, 1999,274(31):21491
  • 6Kleiner DE, Stetler-Stevenson WG. Quantiative zymography:detection of picogram quantities of gelatinase[J]. Anal Biochem, 1994,218:325
  • 7Brinckerhoff CE,Sporn MB. Retinoid and rexinoid for the 21st century: a brave new world for arthritis[J]. J Rheumatol, 2003,30:211
  • 8Konttinen YT, Ceponis A, Takagi M, et al. New collagenolytic enzymes/cas cade identified at the pannus-hard tissue junction in rheumatoid arthritis:de struction from above[.J]. Matrix Biol, 1998,17:585
  • 9Xiao Z, Brownawell AM, Macara IG, et al. A novel nuclear export signal in Smad1 is essential for its signaling activity[J]. J Biol Chem, 2003,278(36):34245
  • 10Yuan W,Varga J.Transforming growth factor-beta repression of matrix metalloproteinase-1 in dermal fibroblast involves Smad3[J]. J Biol Chem, 2001,276(42):38502

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