Smooth muscle specific deletion of N-deacetylase-N-sulfotransferase 1 (Ndst1) results in increased arterial elasticity in mice

The hypothesis tested was that loss of Ndst1 in smooth muscle would lead to significant changes in gene expression and alter functional properties in large and small vessels. The increase in aortic elasticity was increased in mice lacking Ndst1 was associated with significant changes in genes that modify mechano-sensing, contractility and elasticity. Total RNA extracted from aorta from smooth muscle specific Ndst1 deficient mice (SM22αcre+Ndst1-/-) was compared to aorta from wild type (WT, SM22αcre-Ndst1wt/wt ) control mice.