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Vitronectin regulates smooth muscle contractility via alphav and beta1 integrin
1Division of Neurosciences, Beckman Research Institute of the City of Hope, Duarte, CA 91010, USA.
Journal of Cell Science
|June 4, 1998
Summary
Serum and vitronectin in blood can cause smooth muscle cells to lose their contractility by altering their phenotype. This suggests smooth muscle requires protection from blood components in vivo.
Area of Science:
- Cell Biology
- Biochemistry
- Physiology
Background:
- Previous research established methods for maintaining avian smooth muscle contractility in vitro.
- Serum is known to significantly impact cell behavior and function.
Purpose of the Study:
- To investigate the effects of serum and specific plasma components on smooth muscle contractility and phenotype.
- To identify the molecular mechanisms underlying serum-induced changes in smooth muscle.
Main Methods:
- Dissociated avian smooth muscle cells were cultured in a defined medium.
- Experiments involved treatment with serum, purified vitronectin, and blocking antibodies.
- Integrin function was assessed using RGD-sensitive peptides and function-blocking antibodies.
Main Results:
- Serum dramatically altered smooth muscle phenotype, leading to a loss of contractility.
- Vitronectin mimicked serum effects, acting through an RGD-sensitive integrin.
- The integrin alphavbeta1 was identified as the primary receptor for vitronectin-induced phenotypic changes.
- Vitronectin's presence was essential for serum-induced loss of contractility.
Conclusions:
- Smooth muscle cells lose contractility and change phenotype due to serum components like vitronectin.
- The integrin alphavbeta1 mediates vitronectin's effects on smooth muscle.
- In vivo, smooth muscle likely requires protection from abundant blood constituents such as vitronectin.
- These findings have implications for smooth muscle diseases including atherosclerosis, restenosis, and Kaposi's sarcoma.
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