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. (7th May 2013)
- Record Type:
- Journal Article
- Title:
- 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. (7th May 2013)
- Main Title:
- 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
- Authors:
- Song, K. S.
Choi, J. K.
Ahn, D. W. - Abstract:
- <abstract abstract-type="main" id="apha12104-abs-0001"> <title>Abstract</title> <sec id="apha12104-sec-0001" sec-type="section"> <title>Aims</title> <p>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 H<sub>2</sub>O<sub>2</sub> could induce MUC5AC transcription in a dose‐dependent manner and activate tyrosine phosphatase (SHP)‐2 in human airway epithelial cells.</p> </sec> <sec id="apha12104-sec-0002" sec-type="section"> <title>Methods</title> <p>We performed qRT‐PCR to detect the changes in MUC5AC transcription and dot‐blotting analysis to investigate MUC5AC secretion as regulated by SHP‐2.</p> </sec> <sec id="apha12104-sec-0003" sec-type="section"> <title>Results</title> <p>H<sub>2</sub>O<sub>2</sub> induced MUC5AC transcription in a dose‐dependent manner and dramatically activated SHP‐2. In addition, whereas wild‐type SHP‐2 completely inhibited H<sub>2</sub>O<sub>2</sub>‐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.</p> </sec> <sec<abstract abstract-type="main" id="apha12104-abs-0001"> <title>Abstract</title> <sec id="apha12104-sec-0001" sec-type="section"> <title>Aims</title> <p>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 H<sub>2</sub>O<sub>2</sub> could induce MUC5AC transcription in a dose‐dependent manner and activate tyrosine phosphatase (SHP)‐2 in human airway epithelial cells.</p> </sec> <sec id="apha12104-sec-0002" sec-type="section"> <title>Methods</title> <p>We performed qRT‐PCR to detect the changes in MUC5AC transcription and dot‐blotting analysis to investigate MUC5AC secretion as regulated by SHP‐2.</p> </sec> <sec id="apha12104-sec-0003" sec-type="section"> <title>Results</title> <p>H<sub>2</sub>O<sub>2</sub> induced MUC5AC transcription in a dose‐dependent manner and dramatically activated SHP‐2. In addition, whereas wild‐type SHP‐2 completely inhibited H<sub>2</sub>O<sub>2</sub>‐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.</p> </sec> <sec id="apha12104-sec-0004" sec-type="section"> <title>Conclusion</title> <p>We found that H<sub>2</sub>O<sub>2</sub> induced SHP‐2 activation, which acted as a suppressor in H<sub>2</sub>O<sub>2</sub> signalling to regulate MUC5AC transcription in the airway.</p> </sec> </abstract> … (more)
- Is Part Of:
- Acta physiologica. Volume 208:Number 3(2013:Jul.)
- Journal:
- Acta physiologica
- Issue:
- Volume 208:Number 3(2013:Jul.)
- Issue Display:
- Volume 208, Issue 3 (2013)
- Year:
- 2013
- Volume:
- 208
- Issue:
- 3
- Issue Sort Value:
- 2013-0208-0003-0000
- Page Start:
- 245
- Page End:
- 250
- Publication Date:
- 2013-05-07
- Subjects:
- Physiology -- Periodicals
Physiology -- Research -- Periodicals
612 - Journal URLs:
- http://www.blackwell-synergy.com/loi/aps ↗
http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1748-1716 ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1111/apha.12104 ↗
- Languages:
- English
- ISSNs:
- 1748-1708
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 0650.750000
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 4299.xml