MicroRNA-155 regulates lipopolysaccharide-induced mucin 5AC overproduction via a suppressor of cytokine signaling 1-mediated mechanism in human bronchial epithelial cells.

Autor: Liu C; Division of Respiratory Medicine, Second Affiliated Hospital of Chongqing Medical University, No.74, Linjiang Road, Yuzhong District, Chongqing, 400010, China., Du X; Division of Respiratory Medicine, Second Affiliated Hospital of Chongqing Medical University, No.74, Linjiang Road, Yuzhong District, Chongqing, 400010, China., Zhou X; Division of Respiratory Medicine, Second Affiliated Hospital of Chongqing Medical University, No.74, Linjiang Road, Yuzhong District, Chongqing, 400010, China; Division of Respiratory Medicine, First Affiliated Hospital of Hainan Medical University, No.31, Longhua Road, Longhua District, Haikou, Hainan, 570102, China. Electronic address: zxd999@263.net., Kolosov VP; Far Eastern Scientific Center of Physiology and Pathology of Respiration, Siberian Branch, Russian Academy of Medical Sciences, Blagoveshchensk, 675000, Russia., Perelman JM; Far Eastern Scientific Center of Physiology and Pathology of Respiration, Siberian Branch, Russian Academy of Medical Sciences, Blagoveshchensk, 675000, Russia.
Jazyk: angličtina
Zdroj: Respiratory physiology & neurobiology [Respir Physiol Neurobiol] 2019 Jun; Vol. 264, pp. 12-18. Date of Electronic Publication: 2019 Mar 21.
DOI: 10.1016/j.resp.2019.03.008
Abstrakt: Chronic inflammatory lung diseases accompanied by Gram-negative bacteria infection are characterized by excessive mucin production. Lipopolysaccharide (LPS), the major endotoxin released from Gram-negative bacteria, is a potent inflammatory agonist for mucin overproduction. In this study, we sought to examine whether the toll-like receptor (TLR)-responsive microRNA miR-155 plays a role in LPS-provoked induction of mucin 5AC (MUC5AC) and the potential role of suppressor of cytokine signaling 1 (SOCS1) involved in this process. We found that LPS increased the expression of MUC5AC in association with TLR4-dependent miR-155 induction. The suppression of miR-155 by antagomir led to an excessive production of SOCS1, thereby downregulation of MUC5AC production. Collectively, these data imply that miR-155 is involved in LPS-induced MUC5AC overproduction through a TLR4-dependent manner and thereby the downregulation of SOCS1.
(Copyright © 2019. Published by Elsevier B.V.)
Databáze: MEDLINE
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