Regulation of vascular smooth muscle cell gene expression and phenotype by cyclic GMP and cyclic GMP-dependent protein kinase

Lincoln, Thomas M.; Hassan, Sazzad; Dey, Nupur B.; Browner, Natasha C.; Choi, Chung Sik; Dostmann, Wolfgang Wg

doi:10.1186/2048-4623-3-s2-op018

Cited by 1 publication

(1 citation statement)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…NO inhibits SMC proliferation through the extracellular signal-regulated kinase (ERK) pathway leading to increased protein levels of the cyclin-dependent kinase inhibitor p21 Waf1/Cip1 [ 96 ]. cGMP-dependent protein kinase (PKG) overexpression in synthetic SMC results in phenotypic switching of SMC to a contractile phenotype that expresses contractile markers [ 97 ] (SM-MHC, calponin, α-SM actin) with reduced expression of synthetic phenotype markers (osteopontin, thrombospondin) [ 98 , 99 , 100 , 101 ]. Despite the continuous production of NO through the process of arteriogenesis, the effect of NO on SMC phenotype is not predominant in the next stages of arteriogenesis and is overridden by other factors such as cytokines, growth factors, and the increase of circumferential wall tension.…”

Section: The Effect Of Hemodynamics On Smooth Muscle Cell Phenotype During Arteriogenesismentioning

confidence: 99%

Role of Vascular Smooth Muscle Cell Phenotype Switching in Arteriogenesis

Ashraf

Zen

2021

IJMS

View full text Add to dashboard Cite

Arteriogenesis is one of the primary physiological means by which the circulatory collateral system restores blood flow after significant arterial occlusion in peripheral arterial disease patients. Vascular smooth muscle cells (VSMCs) are the predominant cell type in collateral arteries and respond to altered blood flow and inflammatory conditions after an arterial occlusion by switching their phenotype between quiescent contractile and proliferative synthetic states. Maintaining the contractile state of VSMC is required for collateral vascular function to regulate blood vessel tone and blood flow during arteriogenesis, whereas synthetic SMCs are crucial in the growth and remodeling of the collateral media layer to establish more stable conduit arteries. Timely VSMC phenotype switching requires a set of coordinated actions of molecular and cellular mediators to result in an expansive remodeling of collaterals that restores the blood flow effectively into downstream ischemic tissues. This review overviews the role of VSMC phenotypic switching in the physiological arteriogenesis process and how the VSMC phenotype is affected by the primary triggers of arteriogenesis such as blood flow hemodynamic forces and inflammation. Better understanding the role of VSMC phenotype switching during arteriogenesis can identify novel therapeutic strategies to enhance revascularization in peripheral arterial disease.

show abstract