Endothelial cells in vivo are subjected to hemodynamic forces such as shear stresses by blood flow, and stretch by vessel expansion due to blood pressure change. These forces are known to elicit many physiological responses to maintain vascular tonus. To further investigate the stretch- induced responses and the intracellular signaling pathway in vascular endothelial cells, an application of in vitro mechanical stimulation is required. Using these apparatus, we obtained following data; 1) Stretch induced a transient increase in [Ca2+](i). 2) Cyclic uni-axial stretch aligned endothelial cells perpendicular to the stretch direction. 3) Cyclic uni-axial stretch induced tyrosine phosphorylation of focal adhesion proteins and the stretch-induced morphological change was inhibited by tyrosine kinase inhibitors. 4) Cyclic uni-axial stretch induced re-organization of cytoskeleton and focal adhesion. 5) Antisense experiments revealed that focal adhesion kinase (FAK) plays an important role in the stretch-induced morphological change. These data indicate that we could apply mechanical stretch to endothelial cells reproducibly and quantitatively and could investigate the stretch-induced intracellular signaling pathway using our stretch apparatus.
|Number of pages||6|
|Journal||Japanese journal of medical electronics and biological engineering|
|Publication status||Published - Sept 1 1998|
ASJC Scopus subject areas
- Biomedical Engineering