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  • Showing results for Reticulum[Title] AND Stress[Title] AND Contributes[Title] AND Aortic[Title] AND Stiffening[Title] AND via[Title] AND Proapoptotic[Title] AND Fibrotic[Title] AND Signaling[Title] AND Mechanisms[Title]. Your search for “Endoplasmic Reticulum Stress Contributes to Aortic Stiffening via Proapoptotic and Fibrotic Signaling Mechanisms retrieved no results.
Hypertension. 2014 Mar;63(3):e40-5. doi: 10.1161/HYPERTENSIONAHA.113.02558. Epub 2013 Dec 30.

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

Author information

1
Department of Physiology, Georgia Regents University, 1120 15th St, Augusta, GA 30912. kmspitler@gmail.com.

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 with ER stress inhibitor 4-phenylbutyric acid (100 mg/kg per day, 28 days, [124±6]). There was an increase in aortic apoptosis (fold; 3.0±0.3), collagen content (1.4±0.1), and fibrosis (2.0±0.1) in the tunicamycin-treated rats compared with vehicle-treated rats. Inhibition of ER stress in male Sprague-Dawley rats given Ang II (60 ng/min, osmotic pump, 28 days) and treated with either tauroursodeoxycholic acid or phenylbutyric acid (100 mg/kg per day, i.p., 28 days) led to a 20 mm Hg decrease in blood pressure with either inhibitor compared with Ang II treatment alone. Aortic apoptosis, increased collagen content, and fibrosis in Ang II-treated rats were attenuated with ER stress inhibition. We conclude that ER stress is a new signaling mechanism that contributes to aortic stiffening via promoting apoptosis and fibrosis.

KEYWORDS:

apoptosis; fibrosis; muscle, smooth, vascular; vascular stiffness

PMID:
24379182
PMCID:
PMC4004348
DOI:
10.1161/HYPERTENSIONAHA.113.02558
[Indexed for MEDLINE]
Free PMC Article

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