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Spatial and Temporal Analysis of Active ERK in the C. elegans Germline
Published on: November 29, 2016
Abl regulates smooth muscle cell proliferation by modulating actin dynamics and ERK1/2 activation
Li Jia1, Ruping Wang, Dale D Tang
1Center for Cardiovascular Sciences, Albany Medical College, NY 12208, USA.
American Journal of Physiology. Cell Physiology
|February 4, 2012
Summary
Abl kinase regulates vascular smooth muscle cell proliferation by modulating actin dynamics and ERK1/2 phosphorylation. Abl knockdown attenuated ET-1 and PDGF-induced cell growth and arrested the cell cycle.
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- Abl is a nonreceptor tyrosine kinase involved in cell migration, adhesion, and smooth muscle contraction.
- The specific role of Abl in smooth muscle cell proliferation remained uninvestigated prior to this study.
Purpose of the Study:
- To investigate the role of Abl in vascular smooth muscle cell proliferation.
- To determine the signaling pathways regulated by Abl during mitogenic activation.
Main Methods:
- Generated stable Abl knockdown vascular smooth muscle cells using lentivirus-mediated RNA interference.
- Stimulated cells with endothelin-1 (ET-1) and platelet-derived growth factor (PDGF).
- Assessed cell proliferation, cell cycle progression, and phosphorylation of ERK1/2 and Akt.
Main Results:
- ET-1 and PDGF increased Abl phosphorylation, indicating activation.
- Abl knockdown attenuated ET-1 and PDGF-induced smooth muscle cell proliferation and arrested the cell cycle at G(0)/G(1) to S phase.
- Abl knockdown reduced ERK1/2 phosphorylation but did not affect Akt phosphorylation.
- Inhibition of actin polymerization with latrunculin-A also blocked ERK1/2 phosphorylation.
Conclusions:
- Abl kinase plays a critical role in regulating vascular smooth muscle cell proliferation.
- Abl modulates smooth muscle cell proliferation through actin dynamics and ERK1/2 phosphorylation pathways during mitogenic activation.
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