Src homology 2-containing protein tyrosine phosphatase-2 acts as a negative regulator for MUC5AC transcription via the inhibition of the ERK1/2 MAPK signalling pathway in the airway

Acta Physiol (Oxf). 2013 Jul;208(3):245-50. doi: 10.1111/apha.12104. Epub 2013 May 7.

Abstract

Aims: Mucus hypersecretion has been frequently observed in inflammation respiratory diseases. However, the negative regulators for mucus overproduction have not been readily identified. Our work focused on identifying novel negative regulator that modulates mucus overproduction in the human respiratory system. Herein, we examined whether H2 O2 could induce MUC5AC transcription in a dose-dependent manner and activate tyrosine phosphatase (SHP)-2 in human airway epithelial cells.

Methods: We performed qRT-PCR to detect the changes in MUC5AC transcription and dot-blotting analysis to investigate MUC5AC secretion as regulated by SHP-2.

Results: H2 O2 induced MUC5AC transcription in a dose-dependent manner and dramatically activated SHP-2. In addition, whereas wild-type SHP-2 completely inhibited H2 O2 -induced MUC5AC transcription, siRNA-SHP-2 restored it interestingly, suggesting that SHP-2 may act as a negative regulator for mucus overproduction and hypersecretion in the human respiratory tract. Moreover, SHP-2 inhibited the ERK1/2 MAPK pathway, thus abolishing the signalling for MUC5AC transcription.

Conclusion: We found that H2 O2 induced SHP-2 activation, which acted as a suppressor in H2 O2 signalling to regulate MUC5AC transcription in the airway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carcinoma, Mucoepidermoid
  • Cell Line, Tumor
  • Dose-Response Relationship, Drug
  • Epithelial Cells / cytology
  • Epithelial Cells / drug effects
  • Epithelial Cells / enzymology
  • Gene Knockdown Techniques
  • Humans
  • Hydrogen Peroxide / metabolism
  • Hydrogen Peroxide / pharmacology
  • Lung Neoplasms
  • MAP Kinase Signaling System / drug effects
  • MAP Kinase Signaling System / physiology*
  • Mucin 5AC / genetics*
  • Mucin 5AC / metabolism
  • Oxidants / metabolism
  • Oxidants / pharmacology
  • Oxidative Stress / drug effects
  • Oxidative Stress / physiology
  • Protein Tyrosine Phosphatase, Non-Receptor Type 11 / metabolism*
  • Respiratory Mucosa / cytology
  • Respiratory Mucosa / drug effects
  • Respiratory Mucosa / enzymology*
  • Transcription, Genetic / drug effects
  • Transcription, Genetic / physiology

Substances

  • MUC5AC protein, human
  • Mucin 5AC
  • Oxidants
  • Hydrogen Peroxide
  • PTPN11 protein, human
  • Protein Tyrosine Phosphatase, Non-Receptor Type 11