Endoplasmic reticulum stress contributes to aortic stiffening via proapoptotic and fibrotic signaling mechanisms.

ABSTRACT: Vascular smooth muscle cell apoptosis and collagen synthesis contribute to aortic stiffening. A cellular signaling mechanism contributing to apoptotic and fibrotic events is endoplasmic reticulum (ER) stress. In this study, we tested the hypothesis that induction of ER stress in a normotensive rat would cause profibrotic and apoptotic signaling, thereby contributing to aortic stiffening. Furthermore, we hypothesized that inhibition of ER stress in an angiotensin II (Ang II) model of hypertension would improve aortic stiffening. Induction of ER stress with tunicamycin in normotensive Sprague-Dawley rats (10 μg/kg per day, osmotic pump, 28 days) caused an increase in systolic blood pressure (mm Hg; 160±5) compared with vehicle-treated (127±3) or tunicamycin-treated rats that were cotreated w

SUBMITTER: Spitler KM 

PROVIDER: S-EPMC4004348 | biostudies-literature | 2014 Mar

REPOSITORIES: biostudies-literature