Molecular mechanism of interleukin-13-induced mucus hypersecretion in rat airway.
- Author:
De-peng JIANG
1
;
Victor P KOLOSOV
;
Juliy M PERELMAN
;
Xiang-dong ZHOU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Bronchi; secretion; Female; Hepatocyte Nuclear Factor 3-beta; genetics; metabolism; Interleukin-13; pharmacology; Male; Mucin 5AC; metabolism; Mucus; secretion; RNA, Messenger; genetics; metabolism; Random Allocation; Rats; Rats, Sprague-Dawley; STAT6 Transcription Factor; genetics; metabolism; Signal Transduction; drug effects
- From: Journal of Southern Medical University 2011;31(1):73-76
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of interleukin-13 (IL-13) on mucus secretion in vivo and the possible mechanism.
METHODSThe SD rats were randomly divided into control group, IL-13 group and IL-13 plus SP600125 group. The phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase 1/2 (JNK1/2) and the level of MUC5AC in the lung tissues were examined using Western blotting. RT-PCR was performed to examine the mRNA level of STAT4 and STAT6, and electrophoretic mobility shift assays (EMSA) was used to detect the DNA-binding activities of Forkhead box a2 (FOXA2) and activator protein-1 (AP-1).
RESULTSIL-13 caused a significant increase in MUC5AC and p-JNK1/2 expression, but did not affect the phosphorylation of ERK1/2. The expression of MUC5AC was attenuated after treatment with SP600125. A significant increase in STAT6 was observed in IL-13 group compared with that in the control group, whereas the expression of STAT4 mRNA was not significantly affected. The DNA-binding activity of FOXA2 was down-regulated after IL-13 exposure, which did not affect the DNA-binding activity of AP-1.
CONCLUSIONIL-13 down-regulates mucus secretion via STAT6-FOXA2 pathway in vitro.
