- 作者: Si-Youn Song, Eun Chae Jung, Chang Hoon Bae, Yoon Seok Choi and Yong-Dae Kim
- 作者服務機構: Department of Otorhinolaryngology-Head and Neck Surgery, College of Medicine, Yeungnam University, Daegu, Republic of Korea
- 中文摘要: --
- 英文摘要:
Background:
Among a variety of inflammatory mediators, visfatin is a proinflammatory adipocytokine associated with inflammatory reactions in obesity, metabolic syndrome, chronic inflammatory disease, and autoimmune disease. However, the biological role of visfatin in secretion of major mucins in human airway epithelial cells has not been reported. Therefore, this study was conducted in order to investigate the effect and the brief signaling pathway of visfatin on MUC8 and MUC5B expression in human airway epithelial cells.
Results:
Visfatin significantly induced MUC8 and MUC5B expression. Visfatin significantly activated phosphorylation of p38 MAPK. Treatment with SB203580 (p38 MAPK inhibitor) and knockdown of p38 MAPK by siRNA significantly blocked visfatin-induced MUC8 and MUC5B expression.Visfatin significantly increased ROS formation. Treatment with SB203580 significantly attenuated visfatin-induced ROS formation. Treatment with NAC (ROS scavenger) and DPI (NADPH oxidase inhibitor) significantly attenuated visfatin-induced MUC8 and MUC5B expression. However, treatment with NAC and DPI did not attenuate visfatin-activated phosphorylation of p38 MAPK. Visfatin significantly activated the phosphorylation of NF-kappaB. Treatment with PDTC (NF-kappaB inhibitor) significantly attenuated visfatin-induced MUC8 and MUC5B expression.
Conclusions:
These results suggest that visfatin induces MUC8 and MUC5B expression through p38 MAPK/ROS/NF-kappaB signaling pathway in human airway epithelial cells. - 中文關鍵字: --
- 英文關鍵字: Visfatin, p38 MAPK, ROS, NF-κB, MUC8, MUC5B, Epithelial cell