Endothelial FGFR1 deficiency induces AcSDKP-resistant EndMT by regulating TGFβ signal pathway
10.3760/cma.j.issn.1000-6699.2019.11.009
- VernacularTitle: 内皮细胞成纤维生长因子受体1缺陷所致EndMT调控TGFβ信号通路诱导上皮细胞EMT
- Author:
Qiongying HU
1
;
Chengjin AI
;
Gaolin CHEN
;
Daqian XIONG
Author Information
1. Department of Laboratory Medicine, Teaching Hospital of Chengdu University of T. C.M, Chengdu 610072, China
- Publication Type:Journal Article
- Keywords:
Fibroblast growth factor receptor 1;
Endothelial-to-mesenchymal transition;
Epithelial-to-mesenchymal transition;
Diabetic nephropathies
- From:
Chinese Journal of Endocrinology and Metabolism
2019;35(11):969-972
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the role of fibroblast growth factor receptor(FGFR) 1 in endothelial to-mesenchymal transition(EndMT) and epithelial-to-mesenchymal transition(EMT), and to find out a new strategy to study the vascular endothelial function of diabetic renal fibrosis.
Methods:Culture media from FRS2 knockdown HMVECs was transferred to HK-2 cells. Western blot and immunofluorescence staining were used to measure EMT markers and key moleculars of transforming growth factor(TGFβ).
Results:It was found that the medium from FRS2 siRNA-transfected HMVECs reduced E-cadherin protein levels, increased EMT markers levels, and activated TGFβ signal pathway in HK-2 cells.
Conclusion:Endothelial FGFR1 deficiency-induced EndMT leads to EMT in neighboring cells in a manner dependent on TGFβ1 signaling. Endothelial cell FGFR1 is an important molecule for maintaining endothelial homeostasis and epithelial homeostasis, and seems to be a key target for anti-diabetic renal fibrosis.
