Medicine and Health

Dual role of Ca²⁺-activated Cl⁻ channel transmembrane member 16A in lipopolysaccharide-induced intestinal epithelial barrier dysfunction in vitro

J. Sui, C. Zhang, et al.

This study unveils the intriguing dual role of TMEM16A in intestinal epithelial barrier function amidst LPS-induced damage. Conducted by a team of researchers from Dalian Medical University, the findings reveal how TMEM16A exacerbates dysfunction with low LPS doses while providing protection at higher doses, challenging our understanding of epithelial responses to inflammation.

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Abstract

This study investigated the effects of TMEM16A on intestinal epithelial barrier function in vitro using LPS-induced cell damage in IEC-6 cells. LPS significantly increased TMEM16A expression, potentially via NF-κB and Th1/Th2 cytokines. Low-dose LPS caused tight junction dysregulation, while high-dose LPS induced apoptosis-dependent barrier dysfunction. TMEM16A aggravated barrier dysfunction with low-dose LPS by activating ERK1/MLCK signaling but protected against it with high-dose LPS by activating ERK/Bcl-2/Bax signaling. TMEM16A thus plays a dual role in LPS-induced epithelial dysfunction.

Publisher

Cell Death and Disease

Published On

May 29, 2020

Authors

Jingru Sui, Chi Zhang, Xuesheng Fang, Jianwen Wang, Yu Li, Jingyu Wang, Liang Wang, Jianyi Dong, Zijuan Zhou, Changyi Li, Jun Chen, Tonghui Ma, Dapeng Chen

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