Effect of Shear Stress on Connexin43 (Cx43) Protein Expression in Cultured Arteries

Abstract

Shear stress, the frictional force of blood flow on vessel walls, induces artery dilation and remodeling. Low shear stress is associated with atherosclerosis. Cx43, a gap junction protein found in smooth muscle and/or endothelial cells, is involved in vascular cell‐to‐cell communication. Cx43 is up‐regulated in athero‐prone areas of arteries and by low shear stress in cultured endothelial cells, and genetically decreased Cx43 is associated with decreased atherosclerosis. We tested whether low vs. high shear stress would affect Cx43 expression in cultured arteries. This model results in inward remodeling with low shear stress, which is prevented by high shear stress in an eNOS‐dependent manner. Perfused, pressurized (80 mmHg) murine thoracodorsal arteries were cultured for 16.9‐19.9 hr with high physiological (65 ± 16 dynes/cm2, n=3 pooled) or low (2 ± 1 dynes/cm2, n=3 pooled) shear stress. Using western blotting, we found that differences in shear stress did not alter Cx43 protein (low vs. high: 1.035 : 1), whereas eNOS protein was less in low shear stress arteries (low vs. high: 0.591 : 1), suggesting endothelial dysfunction. These data indicate that despite pathological signs in low shear stress arteries, total Cx43 protein expression is unchanged. Support: APS Undergraduate Fellowship, NIH‐R15HL082647.