Suppressor of Cytokine Signaling-1/STAT1 Regulates Renal Inflammation in Mesangial Proliferative Glomerulonephritis Models

Frontiers in Immunology
Jiuxu BaiXiangmei Chen

Abstract

Mesangial proliferative glomerulonephritis (MsGN) is a significant global threat to public health. Inflammation plays a crucial role in MsGN; however, the underlying mechanism remains unknown. Herein, we demonstrate that suppression of the cytokine signaling-1 (SOCS1)/signal transducer and activator of transcription 1 (STAT1) signaling pathway is associated with renal inflammation and renal injury in MsGN. Using MsGN rat (Thy1.1 GN) and mouse (Habu GN) models, renal SOCS1/STAT1 was determined to be associated with CD4+ T cell infiltration and related cytokines. In vitro, SOCS1 overexpression repressed IFN-γ-induced MHC class II and cytokine levels and STAT1 phosphorylation in mesangial cells. SOCS1 and STAT1 inhibitors significantly inhibited IFN-γ-induced CIITA promoter activity and MHC class II expression. In conclusion, our study emphasizes the pivotal role of the SOCS1/STAT1 axis in the regulation of inflammation in MsGN.

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Citations

Jan 11, 2021·Cellular Immunology·Yinghua ZhaoXiangmei Chen
Jun 23, 2021·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Longfei LiuYingwei Wang
Jul 26, 2021·European Journal of Medical Genetics·Alessio GerussiPietro Invernizzi

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BETA
biopsy
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flow cytometry
flow
ELISA

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ImageJ

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