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Renoprotective Effect of KLF2 on Glomerular Endothelial Dysfunction in Hypertensive Nephropathy

Authors
Bae, EunjinYu, Mi-YeonMoon, Jong-JooKim, Ji-EunLee, SaramHan, Sang-WoongPark, Dong-JunKim, Yon-SuYang, Seung-Hee
Issue Date
Mar-2022
Publisher
Multidisciplinary Digital Publishing Institute (MDPI)
Keywords
angiotensin type-1 receptor; glomerular endothelial cell; hypertension; Kruppel-like factor 2
Citation
Cells, v.11, no.5
Indexed
SCIE
SCOPUS
Journal Title
Cells
Volume
11
Number
5
URI
https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/55654
DOI
10.3390/cells11050762
Abstract
Kruppel-like factor 2 (KLF2) regulates endothelial cell metabolism; endothelial dysfunction is associated with hypertension and is a predictor of atherosclerosis development and cardiovascular events. Here, we investigated the role of KLF2 in hypertensive nephropathy by regulating KLF2 expression in human primary glomerular endothelial cells (hPGECs) and evaluating this expression in the kidney tissues of a 5/6 nephrectomy mouse model as well as patients with hypertension. Hypertension-mimicking devices and KLF2 siRNA were used to downregulate KLF2 expression, while the expression of KLF2 was upregulated by administering simvastatin. After 4 mmHg of pressure was applied on hPGECs for 48 h, KLF2 mRNA expression decreased, while alpha-smooth muscle actin (alpha SMA) mRNA expression increased. Apoptosis and fibrosis rates were increased under pressure, and these phenomena were aggravated following KLF2 knockdown, but were alleviated after simvastatin treatment; additionally, these changes were observed in angiotensin II, angiotensin type-1 receptor (AT1R) mRNA, and interleukin-18 (IL-18), but not in angiotensin type-2 receptor mRNA. Reduced expression of KLF2 in glomerular endothelial cells due to hypertension was found in both 5/6 nephrectomy mice and patients with hypertensive nephropathy. Thus, our study demonstrates that the pressure-induced apoptosis and fibrosis of glomerular endothelial cells result from angiotensin II, AT1R activation, and KLF2 inhibition, and are associated with IL-18.
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