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Regulator of G protein signaling 2 (RGS2) deficiency accelerates the progression of kidney fibrosis

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Author(s)
Hee-Seong JangJee In KimMira NohMan Hee RheeKwon Moo Park
Publication Year
2014
Abstract
The regulator of G protein signaling 2 (RGS2) is a potent negative regulator of Gq protein signals including the angiotensin II (AngII)/AngII receptor signal, which plays a critical role in the progression of fibrosis. However, the role of RGS2 on the progression of kidney fibrosis has not been assessed. Here, we investigated the role of RGS2 in kidney fibrosis induced by unilateral ureteral obstruction (UUO) in mice. UUO resulted in increased expression of RGS2 mRNA and protein in the kidney along with increases of AngII and its type 1 receptor (AT1R) signaling and fibrosis. Furthermore, UUO increased the levels of F4/80, Ly6G, myeloperoxidase, and CXCR4 in the kidneys. RGS2 deficiency significantly enhanced these changes in the kidney. RGS2 deletion in the bone marrow-derived cells by transplanting the bone marrow of RGS2 knock-out mice into wild type mice enhanced UUO-induced kidney fibrosis. Overexpression of RGS2 in HEK293 cells, a human embryonic kidney cell line, and RAW264.7 cells, a monocyte/macrophage line, inhibited the AngII-induced activation of ERK and increase of CXCR4 expression. These findings provide the first evidence that RGS2 negatively regulates the progression of kidney fibrosis following UUO, likely by suppressing fibrogenic and inflammatory responses through the inhibition of AngII/AT1R signaling.

Keywords
Fibrosis;
Angiotensin II;
Inflammation;
RGS;
GPCR signaling
Department
Dept. of Molecular Medicine (분자의학)
Publisher
School of Medicine
Citation
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Vol.1842(9) : 1733-1741, 2014
Type
Article
ISSN
0925-4439
DOI
10.1016/j.bbadis.2014.06.022
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/33703
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