SPDEF ameliorates UUO-induced renal fibrosis by transcriptional activation of NR4A1

Nuclear receptor 4A1 (NR4A1) is a gene that increases the likelihood of chronic kidney disease (CKD) and contributes to its development. Previous research has shown that the SAM pointed domain containing Ets transformation-specific transcription factor (SPDEF) can activate NR4A1, but its mechanism of action in renal fibrosis is not yet clear. In this study, we used adenovirus to create a mouse kidney model with a specific knockdown of NR4A1 gene. Our results showed that the knockdown of NR4A1 can accelerate unilateral ureteral obstruction (UUO)-induced renal fibrosis in mice, and overexpression of NR4A1 can significantly reduce transforming growth factor-β1-induced (TGF-β1) fibrosis in HK-2 cells. Additionally, we found that overexpression of SPDEF can improve UUO-induced renal fibrosis in mice and TGF-β1-induced fibrosis in HK-2 by transcriptionally activating NR4A1. These findings suggest that SPDEF can activate NR4A1 transcriptionally and improve renal fibrosis.

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Publication Details

Journal
Molecular Medicine
Published
2024-12-30
DOI
https://doi.org/10.1186/s10020-024-01030-3
Citations
5
Primary Topic
Nuclear Receptors and Signaling
Type
article
Field-Weighted Citation Impact
1.34

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article

SPDEF ameliorates UUO-induced renal fibrosis by transcriptional activation of NR4A1

Hongshuang Wang, Chang Xu, Ziheng Wei, Yan Zhong et al.
5 citations
Molecular Medicine
Nuclear Receptors and Signaling
1.34
article

SPDEF ameliorates UUO-induced renal fibrosis by transcriptional activation of NR4A1

Hongshuang Wang, Chang Xu, Ziheng Wei, Yan Zhong, Fang Fang, Zheng Wang, Xiangting Wang
article en
5 citations

Abstract

Nuclear receptor 4A1 (NR4A1) is a gene that increases the likelihood of chronic kidney disease (CKD) and contributes to its development. Previous research has shown that the SAM pointed domain containing Ets transformation-specific transcription factor (SPDEF) can activate NR4A1, but its mechanism of action in renal fibrosis is not yet clear. In this study, we used adenovirus to create a mouse kidney model with a specific knockdown of NR4A1 gene. Our results showed that the knockdown of NR4A1 can accelerate unilateral ureteral obstruction (UUO)-induced renal fibrosis in mice, and overexpression of NR4A1 can significantly reduce transforming growth factor-β1-induced (TGF-β1) fibrosis in HK-2 cells. Additionally, we found that overexpression of SPDEF can improve UUO-induced renal fibrosis in mice and TGF-β1-induced fibrosis in HK-2 by transcriptionally activating NR4A1. These findings suggest that SPDEF can activate NR4A1 transcriptionally and improve renal fibrosis.

Molecular MedicineVol. 30(1)
Hebei University of Chinese Medicine (CN), First Affiliated Hospital of Hebei Medical University (CN)
Natural Science Foundation of Hebei Province
Good health and well-being
Openalex Percentile: Top 19%
Nuclear Receptors and Signaling
1.34
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