Retinoid Receptor Expression and all- trans Retinoic Acid–Mediated Growth Inhibition in Vascular Smooth Muscle Cells

Circulation ◽  
1996 ◽  
Vol 93 (10) ◽  
pp. 1886-1895 ◽  
Author(s):  
Joseph M. Miano ◽  
Stavros Topouzis ◽  
Mark W. Majesky ◽  
Eric N. Olson
Keyword(s):  
Smooth Muscle ◽  
Retinoic Acid ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Growth Inhibition ◽  
Vascular Smooth Muscle Cells ◽  
Receptor Expression ◽  
Retinoid Receptor ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid

Effect of all-trans retinoic acid and pentagalloyl glucose on smooth muscle cell elastogenesis

2021 ◽  
pp. 1-13
Author(s):  
Kaveh Sanaei ◽  
Sydney Plotner ◽  
Anson Oommen Jacob ◽  
Jaime Ramirez-Vick ◽  
Narendra Vyavahare ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Retinoic Acid ◽  
Smooth Muscle Cells ◽  
Blood Vessels ◽  
Muscle Cells ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Tissue Engineered Blood Vessels ◽  
Pentagalloyl Glucose ◽  
Vitamin A Derivative

BACKGROUND: The main objective of tissue engineering is to fabricate a tissue construct that mimics native tissue both biologically and mechanically. A recurring problem for tissue-engineered blood vessels (TEBV) is deficient elastogenesis from seeded smooth muscle cells. Elastin is an integral mechanical component in blood vessels, allowing elastic deformation and retraction in response to the shear and pulsatile forces of the cardiac system. OBJECTIVE: The goal of this research is to assess the effect of the vitamin A derivative all-trans retinoic acid (RA) and polyphenol pentagalloyl glucose (PGG) on the expression of elastin in human aortic smooth muscle cells (hASMC). METHODS: A polycaprolactone (PCL) and the gelatin polymer composite was electrospun and doped with RA and PGG. The scaffolds were subsequently seeded with hASMCs and incubated for five weeks. The resulting tissue-engineered constructs were evaluated using qPCR and Fastin assay for their elastin expression and deposition. RESULTS: All treatments showed an increased elastin expression compared to the control, with PGG treatments showing a significant increase in gene expression and elastin deposition.

Abstract 638: Urotensin II Promotes Calcification in Vascular Smooth Muscle Cells

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Isabella Albanese ◽  
Zhipeng You ◽  
Bin Yu ◽  
Bianca Barratt ◽  
Dominique Shum-Tim ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Receptor Expression ◽  
Urotensin Ii ◽  
Aortic Valves ◽  
Receptor System ◽  
Positive Correlations

Introduction: Atherosclerosis is a leading cause of death in Western societies. Vasoactive peptide urotensin II (UII) is upregulated in atherosclerosis and several other cardiovascular diseases however further research is required to develop a complete understanding of UII’s role in the pathogenesis of atherosclerosis. Hypothesis: We hypothesized that UII stimulates calcification in vascular smooth muscle cells and that UII, urotensin II related peptide (URP) and UT receptor expression are upregulated in calcified aortic valves. Methods and Results: Human aortic smooth muscle cells (HASMC) were cultured in phosphate media (2.6mmol/L) for 13 days in the presence of varying concentrations of UII (0, 10, 50, 100nm) and the amount of calcium was measured with a calcium assay kit. Protein was extracted and measured with a protein assay kit. HASMC calcification was assessed as the ratio of calcium (μg)/protein (mg). HASMC calcification increased with increasing UII concentration and was significantly elevated in 100nm of UII (N=6, P<0.05) 13 days after incubation. We also examined UII, URP and UT protein expression in 90 carotid endarterectomies and 87 mitral, non-calcified and calcified aortic valves by immunohistochemistry. Multivariant Spearman correlation analyses in carotids revealed significant positive correlations between UII, URP and UT overall staining with calcification, remodeling and inflammation (P<0.05). In valves there was significant positive correlations between UII, URP and UT overall staining with calcification, fibrosis, remodeling, inflammation, lipid score and microvessels (P<0.05). Conclusion: The stimulatory effect of UII on vascular smooth muscle cell calcification as well as the upregulated expression of UII, URP and UT in calcified aortic valves suggests that the UT receptor system plays a key role in the pathogenesis of atherosclerosis and valve calcification.

K depletion alters angiotensin II receptor expression in vascular smooth muscle cells

1990 ◽  
Vol 258 (5) ◽  
pp. C849-C854 ◽  
Author(s):  
S. L. Linas ◽  
R. Marzec-Calvert ◽  
M. E. Ullian
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Receptor Expression ◽  
Ang Ii ◽  
Surface Receptors ◽  
K Depletion

Dietary K depletion (KD) results in increases in the number of angiotensin II (ANG II) receptors and prevents ANG II-induced downregulation of ANG II receptors in membrane preparations of vessels from KD animals. Because dietary KD results in changes in factors other than K, we K depleted vascular smooth muscle cells (VSMC) in culture to determine the specific effects of KD on ANG II receptor expression and processing. Scatchard analysis of ANG II uptake at 4 degrees C revealed that the number of surface receptors was increased by 37% in cells in which K had been reduced by 45%. This increase also occurred in the presence of cycloheximide. To determine the effect of KD on receptor processing, we measured the number of surface receptors after exposure to ANG II in concentrations sufficient to cause down-regulation. After 30-min exposure to ANG II, the number of surface receptors was reduced by 63% in control cells but only 33% in KD cells. Thirty minutes after withdrawing ANG II, surface binding returned to basal levels in control cells but was still reduced by 20% in KD cells. To determine the functional significance of impaired receptor processing, we measured ANG II uptake at 21 degrees C. Uptake at 21 degrees C depends on the functional number of receptors, i.e., the absolute number of surface receptors and the rate at which receptors are recycled to the surface after ANG II binding. ANG II uptake at 21 degrees C was reduced by 50% in KD cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Sign in / Sign up

Export Citation Format

Share Document