Xu W D, Leroy E C, Smith E A
Department of Medicine, Medical University of South Carolina, Charleston 29425.
J Rheumatol. 1991 Feb;18(2):241-6.
To determine whether enhanced matrix synthesis by systemic sclerosis (SSc) fibroblasts in vitro is due to increased responsiveness to transforming growth factor-beta (TGF-beta), fibronectin release by SSc and normal fibroblasts (7 pairs) was measured at various concentrations of TGF-beta. In the absence of TGF-beta, SSc fibroblasts released 30 +/- 22% more fibronectin than normal fibroblasts. While both SSc and normal fibroblasts increased fibronectin release at all concentrations of TGF-beta tested, the percentage increases were not statistically greater for the SSc fibroblasts even though 4 of the SSc fibroblasts strains were selectively sensitive to low concentrations of TGF-beta. TGF-beta increased cell numbers of both SSc and normal strains equally. Our data confirm abnormal regulation of fibronectin gene expression in SSc fibroblasts and suggest increased sensitivity to TGF-beta by some SSc fibroblast strains.
为了确定系统性硬化症（SSc）成纤维细胞在体外增强的基质合成是否归因于对转化生长因子-β（TGF-β）反应性的增加，在不同浓度的TGF-β条件下，对SSc成纤维细胞和正常成纤维细胞（7对）的纤连蛋白释放量进行了测定。在不存在TGF-β的情况下，SSc成纤维细胞释放的纤连蛋白比正常成纤维细胞多30±22%。虽然在所有测试的TGF-β浓度下，SSc成纤维细胞和正常成纤维细胞的纤连蛋白释放量均增加，但即使4株SSc成纤维细胞对低浓度的TGF-β具有选择性敏感性，其增加的百分比在统计学上也并不高于正常成纤维细胞。TGF-β对SSc和正常细胞株的细胞数量增加作用相同。我们的数据证实了SSc成纤维细胞中纤连蛋白基因表达的异常调控，并表明一些SSc成纤维细胞株对TGF-β的敏感性增加。
