Resveratrol Inhibits Aortic Root Dilatation in the Fbn1 ^C1039G/+ Marfan Mouse Model

Abstract

Supplemental Digital Content is available in the text.

RING finger protein 10 attenuates vascular restenosis by inhibiting vascular smooth muscle cell hyperproliferation in vivo and vitro

“…Total RNA was extracted from the carotid arteries by use of TRIzol reagent (TaKaRa Bio Inc., Kusatsu, Japan), and 1 μg of total RNA was reversely transcribed into cDNA according to the manufacturer's directions (TaKaRa Bio Inc., Kusatsu, Japan) (18). The cycle threshold values were measured on the level of β-actin, and the corresponding gene expression was assessed by the 2 −ΔΔCq method.…”

“…In addition, AP-1 is a heterodimer composed of c-Fos and c-Jun, which is also involved in the process of cell cycle, apoptosis, and proliferation. It is reported that AP-1 could induce proliferation and differentiation in a variety of cells (16)(17)(18). However, the relationship among the RNF10, Meox2, or AP-1 signaling proteins during VSMC proliferation has been not unknown.…”

Aortic Aneurysms

“…These include AT1 receptor blockade, 109,111,112 caspase inhibition, 113 and administration of resveratrol. 114 Although TGF-β signaling activation has been postulated in the aortic pathologies, 102,115 whether inhibition of TGF-β preventing or augmenting TAA in Marfan mouse models has not been consistently reported in the literature. 109,112,116 …”

Inhibition of Angiotensin II Dependent AT1a Receptor Stimulation Attenuates Thoracic Aortic Pathology in Fibrillin-1C1041G/+Mice

“…Using pharmacological tools to manipulate the renin angiotensin system, there have been consistent demonstrations that losartan attenuates aortic pathology in mice with fibrillin-1 manipulations. [5][6][7][8][26][27][28] However, it has been proposed that losartan may exert these beneficial actions independent of AT1 receptor antagonism. [6][7][8] Additionally, it has been suggested that AngII may not be responsible for cardiovascular pathology in mice with genetically manipulated fibrillin-1.…”

“…In humans, randomized control trials of angiotensin receptor blockers have yielded mixed results in Marfan syndrome associated TAA, in contrast to the consistent results that have been generated using mouse models of the disease. [5][6][7][8][26][27][28] Most of the mouse and human studies have been performed using losartan, which is characterized by a relatively short half-life and surmountable antagonism. The deficiencies of this drug were likely to have been ameliorated in mouse studies by consistent delivery, via osmotic pumps and diet, leading to a persistent inhibition.…”