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Published on: May 19, 2016
Stretch-induced cell proliferation is mediated by FAK-MAPK pathway
Ju Guang Wang1, Motoi Miyazu, Peng Xiang
1Research Center of Stem Cells Biology and Tissue Engineering, Sun Yat-Sen University, 74 Zhong Shan Road 2, Guang Zhou 510080, China. Juguangw@hotmail.com
Mechanical stretch triggers fibroblast proliferation through focal adhesion kinase (FAK) and mitogen-activated protein kinase (MAPK) pathways. This study confirms FAK and MAPK activation are crucial for stretch-induced cell growth.
Area of Science:
- Cell Biology
- Mechanobiology
- Biochemistry
Background:
- Mechanical forces significantly influence cellular behavior.
- Previous work demonstrated that uni-axial cyclic stretch activates focal adhesion kinase (FAK) and mitogen-activated protein kinase (MAPK) in fibroblasts.
Purpose of the Study:
- To investigate the role of stretch-induced mitogen-activated protein kinase (MAPK) activation in fibroblast proliferation.
- To elucidate the involvement of focal adhesion kinase (FAK) in this process.
Main Methods:
- 3Y1 fibroblasts were subjected to uni-axial cyclic stretch (1 Hz, 120% length).
- Cell proliferation was assessed by bromodeoxyuridine (BrdU) incorporation.
- FAK mutants lacking tyrosine phosphorylation sites were expressed, and MAPK inhibitors (PD98059, SB203580) were used.
Main Results:
- Stretch-induced BrdU incorporation, indicating proliferation, increased significantly within 6 hours.
- Expression of FAK mutants, but not wild-type FAK, blocked stretch-induced BrdU incorporation.
- MAPK inhibitors blocked both MAPK phosphorylation and stretch-induced BrdU incorporation.
Conclusions:
- Stretch-induced focal adhesion kinase (FAK) activation is essential for fibroblast proliferation.
- Subsequent mitogen-activated protein kinase (MAPK) activation plays a critical role in mediating this proliferation.
- These findings highlight the FAK-MAPK signaling axis in mechanotransduction leading to cell growth.
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