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Article

Endothelial Cell-Specific Molecule 1 Promotes Endothelial to Mesenchymal Transition in Renal Fibrosis

1
Division of Nephrology, Department of Medicine, Chung Shan Medical University Hospital, Taichung 40201, Taiwan
2
School of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan
3
Institute of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan
4
Department of Medicine Research, Buddhist Dalin Tzu Chi Hospital, Chiayi 62247, Taiwan
5
Department of Biochemistry, School of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan
6
Clinical Laboratory, Chung Shan Medical University Hospital, Taichung 40201, Taiwan
7
School of Medicine, Tzu Chi University, Hualien 97010, Taiwan
8
Division of Nephrology, Department of Internal Medicine, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chiayi 62247, Taiwan
*
Authors to whom correspondence should be addressed.
These authors contributed equally to this work.
Received: 14 June 2020 / Revised: 27 July 2020 / Accepted: 4 August 2020 / Published: 6 August 2020
(This article belongs to the Special Issue Chronic Kidney Disease (CKD) Studies on Humans and Animals)
The endothelial-to-mesenchymal transition (EndoMT) is involved in the complex pathogenesis of renal fibrosis. The soluble proteoglycan endothelial cell-specific molecule 1 (ESM1) is significantly upregulated in many tumor cells and cirrhosis-related disease. The role of ESM1 in renal fibrosis is unknown. This study investigates the role of ESM1 in renal fibrosis, using an in vivo unilateral ureteral obstruction (UUO) mouse model of renal fibrosis and in vitro mouse kidney MES 13 cells overexpressing ESM1. We observed that ESM1 overexpression significantly increased the motility and migration of MES 13 cells, independent of cell viability. In ESM1-overexpressing MES 13 cells, we also observed elevated expression of mesenchymal markers (N-cadherin, vimentin, matrix metallopeptidase 9 (MMP9)) and the fibrosis marker α-smooth muscle actin (α-SMA) and decreased expression of the endothelial marker vascular endothelial cadherin (VE-cadherin) and CD31. In a mouse model of fibrosis induced by unilateral ureter obstruction, we observed time-dependent increases in ESM1, α-SMA, and vimentin expression and renal interstitial collagen fibers in kidney tissue samples. These results suggest that ESM1 may serve as an EndoMT marker of renal fibrosis progression. View Full-Text
Keywords: endothelial-to-mesenchymal transition; renal fibrosis; endothelial cell specific molecule 1; motility; migration; unilateral ureter obstruction endothelial-to-mesenchymal transition; renal fibrosis; endothelial cell specific molecule 1; motility; migration; unilateral ureter obstruction
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MDPI and ACS Style

Hung, T.-W.; Chu, C.-Y.; Yu, C.-L.; Lee, C.-C.; Hsu, L.-S.; Chen, Y.-S.; Hsieh, Y.-H.; Tsai, J.-P. Endothelial Cell-Specific Molecule 1 Promotes Endothelial to Mesenchymal Transition in Renal Fibrosis. Toxins 2020, 12, 506. https://0-doi-org.brum.beds.ac.uk/10.3390/toxins12080506

AMA Style

Hung T-W, Chu C-Y, Yu C-L, Lee C-C, Hsu L-S, Chen Y-S, Hsieh Y-H, Tsai J-P. Endothelial Cell-Specific Molecule 1 Promotes Endothelial to Mesenchymal Transition in Renal Fibrosis. Toxins. 2020; 12(8):506. https://0-doi-org.brum.beds.ac.uk/10.3390/toxins12080506

Chicago/Turabian Style

Hung, Tung-Wei, Chao-Yang Chu, Chen-Lin Yu, Chu-Che Lee, Li-Sung Hsu, Yong-Syuan Chen, Yi-Hsien Hsieh, and Jen-Pi Tsai. 2020. "Endothelial Cell-Specific Molecule 1 Promotes Endothelial to Mesenchymal Transition in Renal Fibrosis" Toxins 12, no. 8: 506. https://0-doi-org.brum.beds.ac.uk/10.3390/toxins12080506

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