Leptin up-regulates MUC5B expression in human airway epithelial cells via mitogen-activated protein kinase pathway
- Leptin up-regulates MUC5B expression in human airway epithelial cells via mitogen-activated protein kinase pathway
- 김용대; 우현재[우현재]; 유우종[유우종]; 배창훈; 송시연; 김용운; 박소영
- MUCIN GENE-EXPRESSION; LUMINAL LEPTIN; NASAL POLYPS; INTERLEUKIN-1-BETA; PHYSIOLOGY; SECRETION; IMMUNITY; RECEPTOR
- Issue Date
- TAYLOR & FRANCIS INC
- EXPERIMENTAL LUNG RESEARCH, v.36, no.5, pp.262 - 269
- Leptin, an adipocyte-secreted hormone that regulates food intake and metabolic response, has been recently reported to increase in the serum during inflammatory airway disease associated with mucus-hypersecretion. We investigated the effects of leptin on mucin expression in human airway epithelial cells and the signaling pathways. The expression of the leptin receptor was evaluated in human nasal mucosa and NCI-H292 cells. Leptin-induced expression of major respiratory mucins in NCI-H292 cells was analyzed. Mutant leptin, which acts as a receptor antagonist, and specific inhibitors of extracellular signal-regulated kinase (ERK1/2), p38 and Janus kinase-2 (JAK2)/signal transducer and activator of transcription-3 (STAT3) were used. Leptin receptors were expressed in the nasal mucosa and NCI-H292 cells. Treatment with leptin significantly increased the expression of MUC5AC and MUC5B in NCI-H292 cells; these effects were blocked by mutant leptin. The cells activated by leptin showed increased ERK1/2, p38, and STAT3 phosphorylation. Leptin-induced MUC5B expression was blocked by the ERK1/2 and p38 pathway inhibitors, but not by the JAK2/STAT3 pathway inhibitor. Leptin might significantly contribute to the production of major gel-forming mucins by direct stimulation of airway epithelial cells and the activation of leptin receptors coupled with the activation of ERK1/2 or p38, but not the JAK2/STAT3 pathway.
- Appears in Collections:
- 의과대학 > 이비인후과학교실 > Articles
의과대학 > 생리학교실 > Articles
- Files in This Item:
There are no files associated with this item.
- RIS (EndNote)
- XLS (Excel)