Cyclic Strain and Hypertension Increase Osteopontin Expression in the Aorta.

Hypertension has a direct impact on vascular hypertrophy and is a known risk factor for the development of atherosclerosis. Osteopontin (OPN) has emerged as an important protein mediator of inflammation and remodeling of large arteries. However, its role and mechanism of regulation in the setting of hypertension is still unknown.

The role of osteopontin in recovery from hind limb ischemia.

Objective: Osteopontin (OPN) is a highly phosphorylated extracellular matrix glycoprotein that is involved in a diversity of biological processes. In the vascular wall, OPN is produced by monocytes/macrophages, endothelial cells, and smooth muscle cells, and it is thought to mediate adhesion, migration, and survival of these cell types. In this study, we hypothesized that OPN plays a critical role in recovery from limb ischemia.

Mechanoregulation of monocyte chemoattractant protein-1 expression in rat vascular smooth muscle cells.

The authors have previously shown that arterial wall strain mediates the development of vessel wall inflammation in experimental hypertension. The current studies explore the mechanoregulation of monocyte chemoattractant protein-1 (MCP-1), a potent pro-inflammatory chemokine, by mitogen-activated protein kinases (MAPK) and oxidative stress. Rat aortic smooth muscle (RASM) cells were subjected to cyclic strain on a uniform biaxial strain device.

Genetic polymorphisms and oxidative stress in heart failure.

Heart failure results from various known cardiovascular diseases, such as coronary artery disease, or can be the result of an idiopathic dilated cardiomyopathy. It is of utmost importance for diagnostic, preventive, and therapeutic purposes to understand the cellular events that trigger the cascade of functional and structural changes that result in the development and progression of heart failure. Progress in unraveling the genetic background in both ischemic and nonischemic cardiomyopathies has been slow compared with that for monogenic diseases, such as some forms of hypertrophic cardiomyopathy or familial dilated cardiomyopathies.