• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Cellular Physiology >Isoform-specific effects of transforming growth factor on endothelial-to-mesenchymal transition
【24h】

Isoform-specific effects of transforming growth factor on endothelial-to-mesenchymal transition

机译：Isoform-specific转变经济增长的影响因素endothelial-to-mesenchymal过渡

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

Endothelial-to-mesenchymal transition (EndMT) was first reported in the embryogenesis. Recent studies show that EndMT also occurs in the disease progression of atherosclerosis, cardiac and pulmonary fibrosis, pulmonary hypertension, diabetic nephropathy, and cancer. Although transforming growth factor (TGF) is crucial for EndMT, it is not clear which isoform elicits a predominant effect. The current study aims to directly compare the dose-dependent effects of TGF1, TGF2, and TGF3 on EndMT and characterize the underlying mechanisms. In our results, all three TGF isoforms induced EndMT in human microvascular endothelial cells after 72hr, as evidenced by the increased expression of mesenchymal markers N-cadherin and -smooth muscle actinas well as the decreased expression of endothelial nitric oxide synthase. Interestingly, the effect of TGF2 was the most pronounced. At 1ng/ml, only TGF2 treatment resulted in significantly increased phosphorylation (activation) of Smad2/3 and p38-MAPK and increased expression of mesenchymal transcription factorsSnail and FoxC2. Intriguingly, we observed that treatment with 1ng/ml TGF1 and TGF3, but not TGF2, resulted in an increased expression of TGF2, thus indicating that EndMT with TGF1 and TGF3 treatments was due to the secondary effects through TGF2 secretion. Furthermore, silencing TGF2 using small interfering RNA blunted the expression of EndMT markers in TGF1- and TGF3-treated cells. Together, our results indicate that TGF2 is the most potent inducer of EndMT and that TGF1- and TGF3-induced EndMT necessitates a paracrine loop involving TGF2.
机译：Endothelial-to-mesenchymal过渡(EndMT)胚胎发生的首次报道。研究表明,EndMT也发生在动脉粥样硬化的疾病进展,心脏肺纤维化,肺动脉高压,糖尿病肾病和癌症。转化生长因子(TGF)是至关重要的EndMT尚不清楚,同种型抒发一个主要效果。直接比较的存在剂量依赖的相关性影响TGF1、TGF2 TGF3 EndMT和描述底层机制。三个TGF亚型诱导EndMT人类72小时后微血管内皮细胞,表达的增加证明了这一点间叶细胞标记N-cadherin和平滑的肌肉actinas表达降低内皮一氧化氮合酶。TGF2最明显的影响。1 ng / ml,只有TGF2治疗导致显著增加磷酸化(激活)Smad2/3 p38-MAPK和间叶细胞的转录表达增加factorsSnail FoxC2。治疗1 ng / ml TGF1 TGF3,但不是TGF2,导致增加的表达TGF2,从而表明EndMT TGF1和TGF3治疗是由于二次效应通过TGF2分泌。TGF2使用小干扰RNA钝化表达EndMT TGF1和标记TGF3-treated细胞。表明TGF2是最有效的诱导物EndMT TGF1——和TGF3-induced EndMT需要涉及TGF2的旁分泌循环。

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