University Park, Pa. --- Cholesterol, dietary fat, drugs and other chemical bio-regulators may get most of the media attention, but Penn State engineers have shown that mechanical forces, including shear stress, stretch and pressure, can play unsuspected but equivalent roles in some aspects of cardiovascular health and disease.
Dr. John Tarbell, distinguished professor of chemical engineering, and associates in Penn State's Biomolecular Transport Dynamics Laboratory, recently showed that there is a one-to-one correspondence between certain effects of shear stress, the frictional force exerted by blood flow, and a growth factor that stimulates the production of new blood vessels. The Penn State group compared the effects of shear stress with that of vascular endothelial growth factor (VEGF) in laboratory tests with both human and bovine blood vessel tissue. VEGF is multifunctional and, in addition to promoting the growth of new blood vessels, it affects the ability of the cells on the interior surface of blood vessels, the endothelium, to allow fluid to pass through to the cells beneath.
The researchers showed that shear stress and VEGF not only cause similar changes in endothelium transport properties but also do so by the same chemical signaling pathways. Each of the tissue types the group investigated produces nitric oxide in response to shear stress, and nitric oxide is believed to be a key intermediate in the cell signaling cascade for both shear stress and VEGF, according to their recent paper.
Tarbell, who directs Penn State's Biomolecular Transport Dynamics Option for graduate study in the Life Sciences Consortium, notes that his group also investigates the effects of fluid flow as it passes across blood vessel walls. This transmural flow is six orders of magnitude or a million times slower than blood flow and amounts to a "seepage" through the wall's tissue matrix.