Targeted Deletion of EPHX2 in Intestinal Epithelial Cells Alleviates DSS‐Induced Colitis by Enhancing Goblet Cell Differentiation

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Auteurs principaux: Jiuheng Yin, Duoli Zhang, Hongxiang Zeng, Ting Wang, Xi Li
Format: Artículo Open Access
Publié: Wiley 2025
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author Jiuheng Yin
Duoli Zhang
Hongxiang Zeng
Ting Wang
Xi Li
author_facet Jiuheng Yin
Duoli Zhang
Hongxiang Zeng
Ting Wang
Xi Li
Jiuheng Yin
Duoli Zhang
Hongxiang Zeng
Ting Wang
Xi Li
collection Wiley Open Access
contents Targeted Deletion of EPHX2 in Intestinal Epithelial Cells Alleviates DSS‐Induced Colitis by Enhancing Goblet Cell Differentiation Jiuheng Yin Duoli Zhang Hongxiang Zeng Ting Wang Xi Li Cell Biology International ABSTRACT Dysregulation of epoxide hydrolase 2 (‌EPHX2) is associated with the pathogenesis of various diseases. However, the functional role of EPHX2 in ulcerative colitis remains unclear. In this study, we demonstrate that EPHX2 plays a critical role in driving the pathological breakdown of barrier integrity in a colitis model. Pharmacological inhibition of EPHX2 significantly ameliorated Dextran Sulfate Sodium (DSS)‐induced colitis. Notably, conditional knockout of EPHX2 in intestinal epithelial cells (IECs) conferred protection against colitis‐associated mucosal damage. Moreover, EPHX2 deletion in IECs led to increased Muc2 expression and a higher number of goblet cells by promoting goblet cell differentiation, while the expression levels of tight junction proteins (ZO‐1, occludin, and claudin‐1) remained unchanged. These findings identify a previously unrecognized role of EPHX2 in IECs and suggest that targeting EPHX2 may represent a promising therapeutic strategy for ulcerative colitis. 10.1002/cbin.70100 http://onlinelibrary.wiley.com/termsAndConditions#vor
doi_str_mv 10.1002/cbin.70100
format Artículo Open Access
id wiley_oa_10_1002_cbin_70100
institution Wiley Open Access
license_str_mv http://onlinelibrary.wiley.com/termsAndConditions#vor
publishDate 2025
publisher Wiley
record_format wiley_oa
spellingShingle Targeted Deletion of EPHX2 in Intestinal Epithelial Cells Alleviates DSS‐Induced Colitis by Enhancing Goblet Cell Differentiation
Jiuheng Yin
Duoli Zhang
Hongxiang Zeng
Ting Wang
Xi Li
Cell Biology International
Targeted Deletion of EPHX2 in Intestinal Epithelial Cells Alleviates DSS‐Induced Colitis by Enhancing Goblet Cell Differentiation Jiuheng Yin Duoli Zhang Hongxiang Zeng Ting Wang Xi Li Cell Biology International ABSTRACT Dysregulation of epoxide hydrolase 2 (‌EPHX2) is associated with the pathogenesis of various diseases. However, the functional role of EPHX2 in ulcerative colitis remains unclear. In this study, we demonstrate that EPHX2 plays a critical role in driving the pathological breakdown of barrier integrity in a colitis model. Pharmacological inhibition of EPHX2 significantly ameliorated Dextran Sulfate Sodium (DSS)‐induced colitis. Notably, conditional knockout of EPHX2 in intestinal epithelial cells (IECs) conferred protection against colitis‐associated mucosal damage. Moreover, EPHX2 deletion in IECs led to increased Muc2 expression and a higher number of goblet cells by promoting goblet cell differentiation, while the expression levels of tight junction proteins (ZO‐1, occludin, and claudin‐1) remained unchanged. These findings identify a previously unrecognized role of EPHX2 in IECs and suggest that targeting EPHX2 may represent a promising therapeutic strategy for ulcerative colitis. 10.1002/cbin.70100 http://onlinelibrary.wiley.com/termsAndConditions#vor
title Targeted Deletion of EPHX2 in Intestinal Epithelial Cells Alleviates DSS‐Induced Colitis by Enhancing Goblet Cell Differentiation
topic Cell Biology International
url https://onlinelibrary.wiley.com/doi/10.1002/cbin.70100