The protective role of PYY in intestinal mucosal defects induced by SATB2 deficiency in inflammatory bowel disease

Impaired colonic mucosal repair is a critical issue in inflammatory bowel diseases (IBD). SATB2 is essential for maintaining colonic epithelial homeostasis, but its role in mucosal repair is unclear. In this study, flow cytometry was used to assess SATB2's role in colonic epithelial repair in a radiation injury model. SATB2 knockout mice exhibited defective epithelial repair, with a marked reduction in goblet and enteroendocrine cells. Mechanistically, SATB2 directly regulated PPAR-γ transcription, and PYY was observed to translocate into the nucleus and promote the transcription of PPAR-γ target genes. In organoids derived from patients with Crohn's disease, PYY supplementation significantly improved epithelial regeneration, outperforming the PPAR-γ agonist rosiglitazone. In conclusion, SATB2 deficiency impairs colonic epithelial repair, which can be rescued by PYY through activation of PPAR-γ-dependent transcription. These findings suggest that PYY may serve as a promising therapeutic molecule to promote epithelial repair in IBD.

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Publication Details

Journal
Cell Death Discovery
Published
2025-05-08
DOI
https://doi.org/10.1038/s41420-025-02511-y
Primary Topic
Digestive system and related health
Type
article
Field-Weighted Citation Impact
0.00

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article

The protective role of PYY in intestinal mucosal defects induced by SATB2 deficiency in inflammatory bowel disease

Wen Tang, Hengli Ni, Jiaying Xu, Ruidong Chen et al.
Cell Death Discovery
Digestive system and related health
article

The protective role of PYY in intestinal mucosal defects induced by SATB2 deficiency in inflammatory bowel disease

Wen Tang, Hengli Ni, Jiaying Xu, Ruidong Chen, Yongyu Chen, Guangxin Duan, Xiao‐Li Li, Xinjuan Fan, Juan Chen, Jianming Li, Yao Liu, Lei Wu, Lina Sun, Qi Sun, Caiyun Lv, Zhong Fan, Qianyun Shi
article en

Abstract

Impaired colonic mucosal repair is a critical issue in inflammatory bowel diseases (IBD). SATB2 is essential for maintaining colonic epithelial homeostasis, but its role in mucosal repair is unclear. In this study, flow cytometry was used to assess SATB2's role in colonic epithelial repair in a radiation injury model. SATB2 knockout mice exhibited defective epithelial repair, with a marked reduction in goblet and enteroendocrine cells. Mechanistically, SATB2 directly regulated PPAR-γ transcription, and PYY was observed to translocate into the nucleus and promote the transcription of PPAR-γ target genes. In organoids derived from patients with Crohn's disease, PYY supplementation significantly improved epithelial regeneration, outperforming the PPAR-γ agonist rosiglitazone. In conclusion, SATB2 deficiency impairs colonic epithelial repair, which can be rescued by PYY through activation of PPAR-γ-dependent transcription. These findings suggest that PYY may serve as a promising therapeutic molecule to promote epithelial repair in IBD.

Cell Death DiscoveryVol. 11(1)
Sun Yat-sen University (CN), Soochow University (CN), Sixth Affiliated Hospital of Sun Yat-sen University (CN), Nanjing Drum Tower Hospital (CN), Second Affiliated Hospital of Soochow University (CN)
Soochow University, Nanjing University, Nanjing Drum Tower Hospital
Good health and well-being
Openalex Percentile: Top 89%
Digestive system and related health
DOIOpen Access PDFOpenAlex
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