Frontiers in cardiovascular medicine · 2025
Inducing hypertension in Myh11 R247C/R247C mice triggers aortic dissections with increased focal adhesion kinase signaling.
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Kwartler Callie S, Wang Shanzhi, Zhou Zhen, Guan Pujun, Yu Yang, Duan Xue-Yan, Zhang Theodore, Chen Jiyuan, Davis Elaine C, Milewicz Dianna M
Аннотация
OBJECTIVE: We sought to determine if hypertension in combination with a "variant of uncertain significance" that disrupts protein function, MYH11 p.Arg247Cys, would induce aortic dissections in a mouse model.
APPROACH AND RESULTS: Administration of L-NAME via drinking water and a high salt diet increased blood pressure in WT and Myh11R247C/R247C mice and triggered type A dissections with cardiac tamponade in 20% of the Myh11R247C/R247C mice. Myh11R247C/R247C aortas have aberrant smooth muscle contractile unit-elastin connections by transmission electron microscopy, along with increased focal adhesion signaling at baseline, which further increases with hypertension.
CONCLUSION: Gene-environment interactions trigger aortic dissections in Myh11R247C/R247C mice.
APPROACH AND RESULTS: Administration of L-NAME via drinking water and a high salt diet increased blood pressure in WT and Myh11R247C/R247C mice and triggered type A dissections with cardiac tamponade in 20% of the Myh11R247C/R247C mice. Myh11R247C/R247C aortas have aberrant smooth muscle contractile unit-elastin connections by transmission electron microscopy, along with increased focal adhesion signaling at baseline, which further increases with hypertension.
CONCLUSION: Gene-environment interactions trigger aortic dissections in Myh11R247C/R247C mice.