Figure 3.
Progerin expression restricted to VSMCs impairs aortic contraction, but VSMC-specific and EC-specific progerin expression is not sufficient to cause defective vessel relaxation. Wire myography was performed in thoracic aorta rings from 14-week-old mice expressing progerin specifically in VSMCs (LmnaLCS/LCSSM22αtg/+) or in ECs (LmnaLCS/LCSTie2tg/+) and in control mice without progerin expression (LmnaLCS/LCS). (A) Contraction induced by phenylephrine (left) and KCl (right) in aortic rings from LmnaLCS/LCSSM22αtg/+ mice and LmnaLCS/LCS controls. (B) Endothelium-dependent vasodilation induced by acetylcholine (left) and endothelium-independent vasodilation induced by diethylamine NONOate (DEA-NO) (right) in aortic rings from LmnaLCS/LCSSM22αtg/+ mice and LmnaLCS/LCS controls. (C) Contraction induced by phenylephrine (left) and KCl (right) in aortic rings from LmnaLCS/LCSTie2tg/+ mice and LmnaLCS/LCS controls. (D) Endothelium-dependent vasodilation induced by acetylcholine (left) and endothelium-independent vasodilation induced by DEA-NO (right) in aortic rings from LmnaLCS/LCSTie2tg/+ mice and LmnaLCS/LCS controls. Statistical differences were analyzed by two-way ANOVA with Bonferroni’s post-hoc test for acethylcholine, DEA-NO, and phenylephrine data, and by two-tailed t-test for KCl data. * p < 0.05; *** p < 0.001.