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Atherosclerosis is a chronic inflammatory process that initiates with accumulation of apolipoprotein B containing lipoproteins (LPs) in the subendothelium (intima), especially in areas where the laminar flow is disturbed. LP retention triggers an inflammatory response leading to activation of endothelial and vascular smooth muscle cells that culminates with recruitment of leukocytes. Atherosclerosis is the leading cause of vascular disease worldwide being its major clinical manifestations ischemic heart disease, ischemic stroke, and peripheral arterial disease. Even though a lot has been done to unravel the role of turbulent flow and mechanotransduction for atherosclerosis development, little is known about the role of plasma membrane (PM) cholesterol in this process. This chapter is going to be focused on exploring what has been done so far to decipher the role of PM cholesterol in regulating actin architecture, cellular mechanical properties, and cellular contractility in muscle and nonmuscle cells.

Role of Membrane Cholesterol in Modulating Actin Architecture and Cellular Contractility