Mary L. Hixon, Carlos Muro-Cacho, Mark W. Wagner, Carlos Obejero-Paz, Elise Millie, Yasushi Fujio, Yasuko Kureishi, Terry Hassold, Kenneth Walsh, Antonio Gualberto
J Clin Invest.
2000;
106(8):1011–1020
doi:10.1172/JCI8252
This article Copyright © 2000, The American Society for Clinical Investigation
Abstract
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V
ascular smooth muscle cells (VSMCs) at capacitance arteries of hypertensive individuals and animals undergo marked age- and blood pressure–dependent polyploidization and hypertrophy. We show here that VSMCs at capacitance arteries of rat models of hypertension display high levels of Akt1/PKB protein and activity. Gene transfer of Akt1 to VSMCs isolated from a normotensive rat strain was sufficient to abrogate the activity of the mitotic spindle cell–cycle checkpoint, promoting polyploidization and hypertrophy. Furthermore, the hypertrophic agent angiotensin II induced VSMC polyploidization in an Akt1-dependent manner. These results demonstrate that Akt1 regulates ploidy levels in VSMCs and contributes to vascular smooth muscle polyploidization and hypertrophy during hypertension.
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