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 (SM22alphacre+Ndst1-/-) was compared to aorta from wild type (WT, SM22alphacre-Ndst1wt/wt ) control mice.本实验所验证的假说为：平滑肌内Ndst1的缺失会引发基因表达的显著改变，并改变大、小血管的功能特性。Ndst1缺失小鼠的主动脉弹性升高现象，与调控机械感知、收缩能力及弹性的基因的显著表达变化密切相关。研究人员将从平滑肌特异性Ndst1敲除小鼠（SM22αcre+Ndst1-/-）主动脉中提取的总RNA，与野生型对照小鼠（WT，SM22αcre-Ndst1wt/wt）主动脉中提取的总RNA进行了对比分析。