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  • Title: alpha 8 Integrin overexpression in de-differentiated vascular smooth muscle cells attenuates migratory activity and restores the characteristics of the differentiated phenotype.
    Author: Zargham R, Touyz RM, Thibault G.
    Journal: Atherosclerosis; 2007 Dec; 195(2):303-12. PubMed ID: 17275006.
    Abstract:
    Loss of the differentiated (contractile) phenotype of vascular smooth muscle cells (VSMCs) heightens their migratory activity. Integrins, as the main integrators of cell-extracellular matrix, regulate different aspects of cell behavior including migration and differentiation. alpha 8 beta 1 Integrin being expressed in cell types with contractile abilities is downregulated during VSMC phenotype modulation. In this report the ability of alpha 8 beta 1 integrin to induce the characteristics of the contractile phenotype as well as suppression of VSMC migratory activity was investigated. Forced expression of alpha 8 integrin in passage-5 rat VSMCs resulted in lower migratory activity. Western blot and immunoconfocal studies revealed that alpha 8 integrin overexpression was associated with the reappearance of VSMC contractile hallmarks including upregulation of contractile markers, assembly of stress fibres, and increased number of focal adhesions. alpha 8 Integrin overexpression in fibroblast-like Rat1 cells also induced SMC-like characteristics. alpha 8 Integrin-induced reappearance of the contractile hallmarks in de-differentiated VSMCs was impaired by RhoA inhibitors. These results provide evidences that alpha 8 integrin overexpression may assist phenotype-modulated VSMCs to revert to the contractile phenotype possibly via RhoA signaling pathway. Our findings suggest a dynamic role for alpha 8 beta 1 integrin to induce contractile phenotype as well as suppression of VSMC migration, a key player during arterial stenosis.
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