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Overexpression of matrix metalloproteinase-2 mediates phenotypic transformation of lens epithelial cells.

机译:基质金属蛋白酶2的过表达介导晶状体上皮细胞的表型转化。

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摘要

Transforming growth factor-beta (TGF-beta) is known to be a causative factor in pathological fibrosis and the metastasis of cancer cells, through effects on molecules of the extracellular matrix (ECM). We evaluated the influence of TGF-beta(1) on the gene expression of matrix metalloproteinase-2 (MMP-2) in lens epithelial cells (LECs). The results showed that TGF-beta(1) induced the expression of mRNA for MMP-2 in LECs. Subsequently, in order to examine the role of MMP-2, we overexpressed MMP-2 in LECs by stable transfection. The MMP-2-overexpressing LECs showed typical indicators of a myofibroblast-like cell phenotype, such as multiple layers of cells, elongated morphology, and expression of alpha-smooth muscle actin. We also showed that an MMP inhibitor blocked the TGF-beta(1)-induced morphological change in LECs. These results demonstrate that MMP-2 plays a role in the transformation of LECs, which has implications for the pathological fibrosis of these cells.
机译:通过影响细胞外基质(ECM)分子,已知转化生长因子-β(TGF-beta)是病理性纤维化和癌细胞转移的病因。我们评估了晶状体上皮细胞(LECs)中基质金属蛋白酶-2(MMP-2)的基因表达的TGF-beta(1)的影响。结果表明,TGF-beta(1)诱导了LECs中MMP-2的mRNA表达。随后,为了检查MMP-2的作用,我们通过稳定转染在LEC中过表达MMP-2。 MMP-2过表达的LEC表现出成肌纤维细胞样细胞表型的典型指标,例如多层细胞,细长的形态和α平滑肌肌动蛋白的表达。我们还表明,MMP抑制剂可阻止TGF-beta(1)诱导的LEC形态变化。这些结果表明,MMP-2在LEC的转化中起作用,这对这些细胞的病理性纤维化具有影响。

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