Regulation of human lung fibroblast C1q-receptors by transforming growth factor-beta and tumor necrosis factor-alpha.
Regulation of human lung fibroblast C1q-receptors by transforming growth factor-beta and tumor necrosis factor-alpha.
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通过转化生长因子-β 和肿瘤坏死因子-α 调节人肺成纤维细胞 C1q 受体。
DOI：
10.1080/019021499270367
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发表时间：
1999
影响因子：
1.7
通讯作者：
Raghu,G
中科院分区：
文献类型：
--
作者：
Lurton,J;Soto,H;Narayanan,AS;Raghu,G
转化生长因子-β（TGF -β）和肿瘤坏死因子-α（TNF -α）是两种多肽介质，据信在特发性肺纤维化（IPF）的演变中起作用。我们已经评估了这两种物质对人肺成纤维细胞中C1 q的胶原（cC 1 q-R）和球状（gC 1 q-R）结构域的受体表达以及对I型胶原的影响。通过在含有新鲜人血清和加热的血浆衍生血清的培养基中培养人肺外植体并基于C1 q结合分离它们，获得C1 q受体表达不同的两个成纤维细胞亚群[Narayanan，Lurton和Raghu：Am J Resp Cell Mol Biol.1998;17：84]。分别称为HH和NL细胞的细胞在无血清条件下暴露于TGF -β和TNF -α.通过原位杂交和北方分析评估mRNA水平，并在SDS -聚丙烯酰胺凝胶电泳和Western印迹后比较蛋白质水平。暴露于TGF -β和TNF -α的NL细胞含有1. 4和1。6倍，而在HH细胞cC 1 q-R mRNA增加2。0和2。四倍。两种细胞中gC 1 q-R mRNA水平的增加程度较低。这些增加没有反映在CC 1 q- R和gC 1 q- R的蛋白水平上，它们与对照组相似或低于对照组。TGF -β和TNF -α也增加了两种细胞中的前胶原[I] mRNA水平。总的来说，TNF -α引起更大的增加，HH成纤维细胞对TGF -β和TNF -α的反应程度高于NL细胞。这些结果表明，TGF -β和TNF -α上调cC 1 q-R和胶原的mRNA水平，而它们对gC 1 q-R mRNA水平没有显著影响。他们还指出不同的人肺成纤维细胞亚群对炎症介质的反应不同。
Transforming growth factor -beta (TGF -beta) and tumor necrosis factor -alpha (TNF -alpha) are two polypeptide mediators which are believed to play a role in the evolution of idiopathic pulmonary fibrosis (IPF) . We have evaluated the effect of these two substances on the expression of receptors for collagen (cC1q - R) and globular (gC1q - R) domains of C1q and on type I collagen in human lung fibroblasts. Two fibroblast subpopulations differing in C1q receptor expression were obtained by culturing human lung explants in medium containing fresh human serum and heated plasma - derived serum and separating them based on C1q binding [Narayanan, Lurton and Raghu: Am J Resp Cell Mol Biol. 1998;17:84]. The cells, referred to as HH and NL cells, respectively, were exposed to TGF -beta and TNF -alpha in serum - free conditions. The levels of mRNA were assessed by in situ hybridization and Northern analysis, and protein levels compared after SDS - polyacrylamide gel electrophoresis and Western blotting. NL cells exposed to TGF -beta and TNF -alpha contained 1. 4 and 1. 6 times as much cC1q - R mRNA, respectively, whereas in HH cells cC1q - R mRNA increased 2. 0 - and 2. 4 - fold. The gC1q - R mRNA levels increased to a lesser extent in both cells. These increases were not reflected in protein levels of CC1q - R and gC1q - R, which were similar to or less than controls. Both TGF -beta and TNF -alpha also increased procollagen [I] mRNA levels in both cells. Overall, TNF -alpha caused a greater increase and the degree of response by HH fibroblasts to both TGF -beta and TNF -alpha was higher than NL cells. These results indicated that TGF -beta and TNF -alpha upregulate the mRNA levels for cC1q - R and collagen and that they do not affect gC1q - R mRNA levels significantly. They also indicated different subsets of human lung fibroblasts respond differently to inflammatory mediators.