TGF-β1 Mediates the EndoMt in High Glucose-Treated Human Retinal Microvascular Endothelial Cells

被引:0
作者
Ying, Jia [1 ]
Wang, Peipei [2 ]
Jin, Xiao [1 ]
Luo, Li [1 ]
Lai, Keshuang [3 ]
Li, Jun [1 ,4 ]
机构
[1] Wenzhou Med Univ, Lishui Municipal Cent Hosp, Affiliated Hosp 5, Dept Ophthalmol, Lishui, Peoples R China
[2] Wenzhou Med Univ, Lishui Municipal Cent Hosp, Affiliated Hosp 5, Dept Stomatol, Lishui, Peoples R China
[3] Yunhe Cty Hosp Tradit Chinese Med, Dept Ophthalmol, Lishui, Peoples R China
[4] Wenzhou Med Univ, Lishui Municipal Cent Hosp, Affiliated Hosp 5, Dept Ophthalmol, 289 Kuocang Rd, Lishui 323000, Peoples R China
关键词
Diabetic retinopathy; EndoMT; Hrmecs; TGF-beta; 1; Vitreoretinal fibrosis; TO-MESENCHYMAL TRANSITION; GROWTH-FACTOR; TGF-BETA; FIBROSIS; BLOCKADE;
D O I
10.1080/08820538.2023.2300806
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
The purpose of our study was to investigate the role of TGF-beta 1 in the endothelial-to-mesenchymal transition (EndoMT) and fibrosis in high glucose (HG)-treated human retinal microvascular endothelial cells (HRMECs). HRMECs were cultured not only under normal glucose (NG) conditions with or without TGF-beta 1, but also under HG conditions with or without the TGF-beta 1 inhibitor SB431542. The expression of TGF-beta 1 was detected by real time-PCR and enzyme-linked immunosorbent assay. Morphological changes and migration of the HRMECs were observed using electron microscopy and scratch-wound assay. Endothelial markers, such as CD31 and vascular endothelial (VE)-cadherin, and the acquisition of fibrotic markers, such as alpha smooth muscle actin (alpha-SMA) and fibroblast-specific protein-1 (FSP-1), were determined by immunofluorescent staining and western blot. The level of TGF-beta 1 was significantly upregulated in HG-treated HRMECs. And HG stimulation promoted obvious morphological changes and the migration ability in HRMECs. Our results also demonstrated increased expression of alpha-SMA and FSP-1, and decreased expression of CD31 and VE-cadherin, in HG-treated HRMECs. These EndoMT-related changes were promoted by TGF-beta 1 and abrogated by SB431542. The results of this study demonstrated the important role of TGF-beta 1 in HG-induced vitreoretinal fibrosis. EndoMT is likely to be involved in the associated effects.
引用
收藏
页码:312 / 319
页数:8
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