• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Animal model of sclerotic skin. V: Increased expression of alpha-smooth muscle actin in fibroblastic cells in bleomycin-induced scleroderma.
【24h】

Animal model of sclerotic skin. V: Increased expression of alpha-smooth muscle actin in fibroblastic cells in bleomycin-induced scleroderma.

机译：硬化性皮肤的动物模型。 V：博莱霉素诱导的硬皮病中成纤维细胞中α-平滑肌肌动蛋白的表达增加。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Scleroderma is a connective tissue disorder with unknown etiology. Myofibroblasts appear during fibrotic processes such as scleroderma, hypertrophic scarring, and wound healing. We previously established a mouse model for scleroderma by local injections of bleomycin. To determine the phenotype of the fibroblasts in sclerotic skin after bleomycin treatment, we examined the expression of alpha-smooth muscle actin (alpha-SMA), a marker for myofibroblasts, in lesional skin as well as in fibrous lung in this model. Dermal sclerosis was induced by daily local injections of bleomycin (100 microg/ml) for 3 weeks in C3H mice. Immunohistochemical examination showed that alpha-SMA-reactive cells were detectable on fibroblastic cells in bleomycin-injected skin at 1 week. There was a significant increase in the immunoreactive fibroblastic cells for alpha-SMA in lesional skin in parallel with the induction of dermal sclerosis. After 3 weeks' treatment with bleomycin, the number of alpha-SMA-reactive fibroblasts showed an 11-fold increase compared with that in control PBS-treated mice. alpha-SMA-positive cells were also detected in lung parenchyma after bleomycin treatment. Following concomitant treatment with anti-transforming growth factor-beta (TGF-beta) antibody with bleomycin, the number of alpha-SMA-positive fibroblastic cells was significantly reduced up to 50%, along with the reduction of dermal sclerosis. To confirm the protein level of alpha-SMA, immunoblotting was carried out. Results showed an increase of alpha-SMA expression in lesional skin at 3 weeks of bleomycin treatment, which was reduced following anti-TGF-beta antibody treatment. These data suggest that fibroblastic cells are phenotypically altered into myofibroblasts during the fibrotic process in the experimental model of bleomycin-induced scleroderma, which was considered mediated, for the most part, by TGF-beta. Blockade of TGF-beta may be a therapeutic intervention for scleroderma. (c)2001 Elsevier Science.
机译：硬皮病是一种病因不明的结缔组织疾病。肌纤维母细胞在纤维化过程中出现，例如硬皮病，肥厚性瘢痕形成和伤口愈合。我们以前通过局部注射博来霉素建立了硬皮病的小鼠模型。为了确定博来霉素治疗后硬化性皮肤中成纤维细胞的表型，我们在该模型的病灶皮肤和纤维肺中检查了α-平滑肌肌动蛋白（α-SMA）（成肌纤维细胞标志物）的表达。在C3H小鼠中，每天局部注射博来霉素（100 microg / ml）诱导3周，从而引起皮肤硬化。免疫组织化学检查显示，注射博来霉素的皮肤在1周时可在成纤维细胞上检测到α-SMA反应性细胞。与诱导皮肤硬化并行，病灶皮肤中针对α-SMA的免疫反应性成纤维细胞显着增加。博来霉素处理3周后，与对照PBS处理的小鼠相比，α-SMA反应性成纤维细胞的数量增加了11倍。博来霉素治疗后在肺实质中也检测到了α-SMA阳性细胞。伴有博来霉素的抗转化生长因子-β（TGF-β）抗体伴随治疗后，α-SMA阳性成纤维细胞的数量显着减少了多达50％，同时皮肤硬化也有所减少。为了确认α-SMA的蛋白质水平，进行了免疫印迹。结果显示，博来霉素治疗3周后，病变皮肤中的α-SMA表达增加，抗TGF-β抗体治疗后减少。这些数据表明，在博来霉素诱导的硬皮病的实验模型中，成纤维细胞在纤维化过程中被表型化为成纤维细胞，这在很大程度上被认为是由TGF-β介导的。阻断TGF-β可能是硬皮病的治疗干预措施。 （c）2001 Elsevier科学。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号