Smooth endocytosis of modified LDL including numerous

Smooth muscle cells are majorly present in hollow organs like heart,liver,kidney etc. They show considerable difference depending on their position in the arterial tree. Due to secretion of insoluble extracellular matrix the cells assume the function of withstanding high blood pressure of the circulating blood in the arterial system. Because of the presence of continuous blood flow the interaction between the cell and the extracellular matrix is very crucial in maintaining vascular integrity. The role of SMC’s is extensively noted in may diseases like monogenic diseases, such as Marfan syndrome, which is responsible for aneurysms and dissections of the ascending aorta, via defects in fibrillin or other molecules, or cerebral microangiopathy, via an intercellular molecular defect in Notch. There are reports suggesting the prominent involvement of SMC’s plasticity which play a role in acetylation/deacetylation and methylation of histones. These epigenetic modifications of histones create changes in DNA accessibility to repressor or enhancer transcription factors which are majorly related to Kruppel-like factor 4, P300, myocardin and serum responsive factor.  SMC’s play a very big role in atherosclerosis, factors like lipoprotein accumulation, endothelial activation and inflammatory responses play a critical role in development of atherosclerotic lesions resulting in phenotypic switching of SMC’s. The SMC’s acquire macrophage like phenotype expressing CD68 positivity which is responsible for endocytic activity. There are reports suggesting the role of SMC’s in foam cell formation and they posses the complete equipment for endocytosis of modified LDL including numerous scavenger receptors. In a study showing 50% foam cells in advanced human coronary artery lesions express smooth muscle ?-actin. These cells also expressed CD68. Most importantly the expression of the cholesterol exporter ATP-binding cassette transporter A1 was reduced in smooth muscle ?-actin+ foam cells as compared to ?-actin- CD68+ cells,  suggesting that the former might express reverse cholesterol transport resulting in plaque cholesterol burden and associated inflammation, leading to atherosclerosis.