Aquaporin 5 expression inhibited by LPS via p38/JNK signaling pathways in SPC-A1 cells.

Abstract

Proper H(2)O to mucin ratio of airway mucus is important for mucociliary clearance. Recent studies suggest that decreased aquaporin 5 (AQP5) is correlated with increased staining of MUC5AC in submucosal glands of COPD patients. Lipopolysaccharide (LPS) is one of the major insults in airway mucin secretion in COPD. In this study, changes in both AQP5 and MUC5AC expression levels in SPC-A1, a human airway submucosal gland cell line, were quantified after exposure of the cells to LPS. AQP5 transcription and protein expression were decreased while MUC5AC expression was increased by LPS exposure in SPC-A1 cells. Further studies revealed that AQP5 expression was down-regulated via the p38/JNK signaling pathway, while MUC5AC was up-regulated through the EGFR-p38/JNK pathway. Therefore, p38 and JNK may become promising targets to preserve AQP5 expression and prevent MUC5AC over-expression to restore proper H(2)O to mucin ratio of the airway mucus, which may be beneficial to the clinical management of COPD patients.

• Authors: Yao Shen, Zhihong Chen, Yuehong Wang, Zhenju Song, Ziqiang Zhang, Meiling Jin, Xiangdong Wang, Chunxue Bai
• Journal: Respiratory physiology & neurobiology (Respir Physiol Neurobiol) Vol. 171 Issue 3 Pg. 212-7 (May 31 2010) ISSN: 1878-1519 [Electronic] Netherlands
• PMID: 20362698 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright 2010 Elsevier B.V. All rights reserved.

Chemical References

• Aquaporin 5
• Lipopolysaccharides
• MUC5AC protein, human
• Mucin 5AC
• RNA, Messenger
• JNK Mitogen-Activated Protein Kinases
• p38 Mitogen-Activated Protein Kinases

Topics

• Aquaporin 5 (biosynthesis)
• Blotting, Western
• Cell Line, Tumor
• Enzyme-Linked Immunosorbent Assay
• Fluorescent Antibody Technique
• Gene Expression (drug effects)
• Humans
• JNK Mitogen-Activated Protein Kinases (drug effects, metabolism)
• Lipopolysaccharides (pharmacology)
• Mucin 5AC (biosynthesis)
• Pulmonary Disease, Chronic Obstructive (metabolism, physiopathology)
• RNA, Messenger (analysis)
• Respiratory Mucosa (drug effects, metabolism)
• Reverse Transcriptase Polymerase Chain Reaction
• Signal Transduction (drug effects, physiology)
• p38 Mitogen-Activated Protein Kinases (drug effects, metabolism)