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4128 are up-regulated in proliferating VSMCs. 130 In addition, joint RTK/integrin complex signaling networks impact G1 phase regulation by inhibiting p21CIP1 and p27KIP1, resulting in Rb phosphorylation and induction of E2F-dependent genes, with ­progression to autonomous stages of the cell cycle (S, G2, and M) that are independent of external stimuli. 37 Migration Smooth muscle migration is an essential element of wound repair, but unchecked migration and proliferation can contribute to ­neointimal thickening and development of atherosclerotic plaques.

In VSMCs, multiple levels of epigenetic controls exist for gene expression leading to differentiation or dedifferentiation programs in healthy cells and for dysregulated gene expression in vascular disease. These epigenetic changes in VSMCs involve both DNA and histone methylation as well as histone acetylation/deacetylation. 55 Acetylation is controlled by HATs, which promote gene transcription by destabilizing chromatin structure to an“open,”transcriptionally active conformation, and HDACs, which promote chromatin condensation to a “closed,” transcriptionally silent conformation with restricted access to DNA.

Coordination of actin dynamics depends upon multiple actin binding and associated proteins for actin filament nucleation and extension (actin-related protein [Arp2/3], WAVE, Wiskott-Aldrich's syndrome [WASP], mDia, profilin) and actin filament depolymerization (cofilin) and filament capping and severing (gelsolin), remodeling events regulated by small G-proteins Rho, Rac, and cdc42 and Rhoactivated protein kinase (ROCK). Myosin II activation by Ca2+/calmodulin (CaM)/myosin light chain kinase (MLCK) and p21-activated kinase (PAK) generates traction forces on the matrix to move the cell forward.

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