4P-1045 Estrogen receptor expression in vascular smooth muscle cells is altered by diabetes: implications for inducible NO synthase function

2003 ◽  
Vol 4 (2) ◽  
pp. 304
Author(s):  
A. Cignarella ◽  
C. Minici ◽  
A. Brusadelli ◽  
C. Bolego ◽  
A. Maggi ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
No Synthase ◽  
Receptor Expression ◽  
Estrogen Receptor Expression ◽  
Inducible No Synthase

scholarly journals Augmented Expression of Inducible NO Synthase in Vascular Smooth Muscle Cells During Aging Is Associated With Enhanced NF-κB Activation

1999 ◽  
Vol 19 (12) ◽  
pp. 2854-2862 ◽  
Author(s):  
Zhong-qun Yan ◽  
Allan Sirsjö ◽  
Marie-Luce Bochaton-Piallat ◽  
Giulio Gabbiani ◽  
Göran K. Hansson
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
No Synthase ◽  
Inducible No Synthase

Estradiol-mediated ERK phosphorylation and apoptosis in vascular smooth muscle cells requires GPR 30

2009 ◽  
Vol 297 (5) ◽  
pp. C1178-C1187 ◽  
Author(s):  
Qingming Ding ◽  
Robert Gros ◽  
Lee E. Limbird ◽  
Jozef Chorazyczewski ◽  
Ross D. Feldman
Keyword(s):  
Estrogen Receptor ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Pi3 Kinase ◽  
Receptor Expression ◽  
Erk Phosphorylation ◽  
Stimulation Of

Recent studies suggest that the rapid and nongenomic effects of estradiol may be mediated through the G protein-coupled receptor dubbed GPR30 receptor. The present study examines the role of GPR30 versus a classical estrogen receptor (ERα) in mediating the growth regulatory effects of estradiol. GPR30 is readily detectable in freshly isolated vascular tissue but barely detectable in cultured vascular smooth muscle cells (VSMC). In freshly isolated aortic tissue, estradiol stimulated extracellular signal-regulated kinases (ERK) phosphorylation. In contrast, in cultured VSMC, where GPR30 expression is significantly reduced, estradiol inhibits ERK phosphorylation. Transfer of the genes encoding GPR30 led to estradiol stimulation of ERK phosphorylation, which is opposite the effects of estradiol in the primary culture of VSMCs. Transduction of the mineralocorticoid receptor (MR) had no effect on estradiol effects on ERK. Estradiol-mediated stimulation of ERK subsequent to heterologous GPR30 expression was pertussis toxin sensitive and phosphoinositide 3-kinase (PI3 kinase) dependent; under these conditions, estradiol also inhibited protein kinase A (PKA). In contrast, in the absence of GPR30 expression in cultured VSMC, estradiol stimulated PKA activity and inhibited ERK phosphorylation. To determine the functional effect of GPR30 (vs. estrogen receptor expression), we assessed estradiol-mediated apoptosis. In the absence of GPR30 expression, estradiol inhibited apoptosis. This effect was enhanced with ERα expression. In contrast, with GPR30 expression, estradiol stimulated apoptosis in an ERK-dependent manner. Thus the effect of estradiol on vascular smooth muscle cell apoptosis is likely dependent on the balance between ER-mediated PKA activation and GPR30-mediated PKA inhibition and PI3 kinase activation. Taken together, we postulate that modulation of GPR30 expression or activity may be an important determinant of the effects of estradiol in the vasculature.

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)

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