The findings were published in the Dec. 28, 2007 issue of the Journal of Biological Chemistry.
Blood vessels contain three important layers the endothelium that lines the vessel walls, the smooth muscle cells responsible for regulating blood flow, and the lumen, the open channel through which blood travels. In healthy young humans, the production of compounds by the cells in these layers remains balanced, allowing for normal vessel function and unrestricted blood flow.
Hassanain developed a transgenic mouse that produces excess human profilin 1 in the smooth muscle cell area with the intent to cause stress in the vessel walls that leads to hypertrophy, or an enlargement of the smooth muscle cells that eventually leads to structural and functional changes in the entire vessel. The mice were developed to test the theory that the impaired regulation of the profilin 1 gene would eventually lead to high blood pressure, and observe how that happens.
Vascular remodeling is a known problem as people get older. Their blood vessels tend to stiffen, even in healthy adults. This causes stress on the vessels, which leads to hypertension, Hassanain said.
At the heart of the vessel activities is a protein called actin within the smooth muscle cells, and its relationship to profilin 1. In the presence of too much profilin1, actin is transformed from a loosely configured protein into a more rigid fibrous state. This change in actin's nature increases the size and the stiffness of smooth muscle cells.
The cells undergo other changes that prepare them for cell divisio
|Contact: Hamdy Hassanain|
Ohio State University