Morehead State University
The Effects of Rho-kinase Inhibition on Alpha-Actin and Beta-Actin Cytoskeletal Remodeling in Resting and Contracting Aortic Smooth Muscle Cells
Institution
Morehead State University
Faculty Advisor/ Mentor
Michael E. Fultz
Abstract
Evidence suggests that differential remodeling of alpha- and beta-actin may explain the unique properties of smooth muscle. It appears that redistribution of alpha-actin to podosomes is sensitive to phorbol-induced stimulation while beta-actin does not remodel into podosomes, but instead remodels to hold cells in a shortened configuration. The mechanisms for regulating this differential remodeling is poorly understood. The effect of Rho-kinase inhibition on both actin domains was examined before and after phorbol (PDBu) stimulation in A7r5 smooth muscle cells. Data suggests that Rho-kinase inhibition blocks the alpha-actin remodeling to the podosomes and stimulates dissolution of the remaining alpha-actin stress cables. Beta-actin remodeling appears to be unaffected. This suggests that Rho-kinase may selectivity regulate alpha-actin remodeling, with little effect on beta-actin. This supports the hypothesis of differential remodeling.
The Effects of Rho-kinase Inhibition on Alpha-Actin and Beta-Actin Cytoskeletal Remodeling in Resting and Contracting Aortic Smooth Muscle Cells
Evidence suggests that differential remodeling of alpha- and beta-actin may explain the unique properties of smooth muscle. It appears that redistribution of alpha-actin to podosomes is sensitive to phorbol-induced stimulation while beta-actin does not remodel into podosomes, but instead remodels to hold cells in a shortened configuration. The mechanisms for regulating this differential remodeling is poorly understood. The effect of Rho-kinase inhibition on both actin domains was examined before and after phorbol (PDBu) stimulation in A7r5 smooth muscle cells. Data suggests that Rho-kinase inhibition blocks the alpha-actin remodeling to the podosomes and stimulates dissolution of the remaining alpha-actin stress cables. Beta-actin remodeling appears to be unaffected. This suggests that Rho-kinase may selectivity regulate alpha-actin remodeling, with little effect on beta-actin. This supports the hypothesis of differential remodeling.