Activation of muscarinic cholinoceptor ameliorates tumor necrosis factor‐α‐induced barrier dysfunction in intestinal epithelial cells | Zendy

Khan Md Rafiqul Islam | Zendy; Uwada Junsuke | Zendy; Yazawa Takashi | Zendy; Islam Md Tariqul | Zendy; Krug Susanne M. | Zendy; Fromm Michael | Zendy; Karaki Shin-ichiro | Zendy; Suzuki Yuichi | Zendy; Kuwahara Atsukazu | Zendy; Yoshiki Hatsumi | Zendy; Sada Kiyonao | Zendy; Muramatsu Ikunobu | Zendy; Anisuzzaman Abu Syed Md | Zendy; Taniguchi Takanobu | Zendy

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Activation of muscarinic cholinoceptor ameliorates tumor necrosis factor‐α‐induced barrier dysfunction in intestinal epithelial cells

Author(s) -

Khan Md Rafiqul Islam,

Uwada Junsuke,

Yazawa Takashi,

Islam Md Tariqul,

Krug Susanne M.,

Fromm Michael,

Karaki Shin-ichiro,

Suzuki Yuichi,

Kuwahara Atsukazu,

Yoshiki Hatsumi,

Sada Kiyonao,

Muramatsu Ikunobu,

Anisuzzaman Abu Syed Md,

Taniguchi Takanobu

Publication year - 2015

Publication title -

febs letters

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.593

H-Index - 257

eISSN - 1873-3468

pISSN - 0014-5793

DOI - 10.1016/j.febslet.2015.10.029

Subject(s) - muscarinic acetylcholine receptor , tumor necrosis factor alpha , chemistry , microbiology and biotechnology , tumor necrosis factor α , cancer research , necrosis , medicine , biology , endocrinology , biochemistry , receptor

Impaired intestinal barrier function is one of the critical issues in inflammatory bowel diseases. The aim of this study is to investigate muscarinic cholinoceptor (mAChR)‐mediated signaling for the amelioration of cytokine‐induced barrier dysfunction in intestinal epithelium. Rat colon challenged with TNF‐α and interferon γ reduced transepithelial electrical resistance (TER). This barrier injury was attenuated by muscarinic stimulation. In HT‐29/B6 intestinal epithelial cells, muscarinic stimulation suppressed TNF‐α‐induced activation of NF‐κB signaling and barrier disruption. Finally, muscarinic stimulation promoted the shedding of TNFR1, which would be a mechanism for the attenuation of TNF‐α/NF‐κB signaling and barrier disruption via mAChR.

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