HGF suppresses the production of collagen type III and α-SMA induced by TGF-β1 in healing fibroblasts
HGF suppresses the production of collagen type III and α-SMA induced by TGF-β1 in healing fibroblasts
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DOI：
10.1007/s00421-008-0733-7
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发表时间：
2008-07-01
影响因子：
3
通讯作者：
Li, Zhaozhu
中科院分区：
文献类型：
--
作者：
Jiang, Dapeng;Jiang, Zhitao;Li, Zhaozhu
本研究的目的是检测HGF在大鼠愈合成纤维细胞中阻断TGF-β 1诱导的胶原III和α-平滑肌肌动蛋白（α-SMA）产生的有效性，成纤维细胞从愈合的内侧副韧带（MCL）损伤中获得。细胞培养物补充有5 ng/ml的TGF-β 1沿着增加剂量的HGF（10-40 ng/ml）。用酶联免疫吸附法测定培养上清中Ⅲ型胶原的含量。通过蛋白质印迹法评估α-SMA的表达。用TGF-β 1治疗显著刺激愈合成纤维细胞中的胶原III和α-SMA产生。值得注意的是，加入HGF以剂量依赖性方式减少了TGF-β 1诱导的所有组分的产生。这项研究表明，HGF在培养的愈合MCL损伤成纤维细胞中有效拮抗TGF-β 1的作用。这些结果为HGF作为MCL瘢痕形成和不良愈合的治疗剂提供了细胞和分子基础。
The aim of this study was to examine the effectiveness of HGF in blocking TGF-beta 1-induced collagen III and alpha-smooth muscle actin (alpha-SMA) production in rat healing fibroblasts, fibroblasts were obtained from healing medial collateral ligament (MCL) injury. Cell culture was supplemented with 5 ng/ml of TGF-beta 1 along with increasing doses of HGF (10-40 ng/ml). The productions of collagen III in supernatants culture were assayed by enzyme-linked immunosorbent assay. Expression of alpha-SMA was assessed by Western blot. Treatment with TGF-beta 1 significantly stimulated collagen III and alpha-SMA production in healing fibroblasts. Remarkably, the addition of HGF reduced productions of all components induced by TGF-beta 1 in a dose-dependent manner. This study shows that HGF antagonizes the action of TGF-beta 1 effectively in cultured healing MCL injury fibroblasts. The results provide a cellular and molecular basis for HGF's acting as a therapeutic agent for MCL scar formation and poor healing.