Mechanical Strain Increases PDGF-B and PDGF β Receptor Expression in Vascular Smooth Muscle Cells

1999 ◽  
Vol 265 (2) ◽  
pp. 606-610 ◽  
Author(s):  
Yunn-Hwa Ma ◽  
Shanhong Ling ◽  
Harlan E. Ives
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Mechanical Strain ◽  
Muscle Cells ◽  
Receptor Expression ◽  
Β Receptor

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)

scholarly journals Agents which increase cyclic AMP have diverse effects on low-density-lipoprotein-receptor function in human vascular smooth-muscle cells and skin fibroblasts

1990 ◽  
Vol 267 (3) ◽  
pp. 607-614 ◽  
Author(s):  
A Middleton ◽  
B Middleton
Keyword(s):  
Smooth Muscle ◽  
Cyclic Amp ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Ldl Receptor ◽  
Muscle Cells ◽  
Skin Fibroblasts ◽  
Receptor Expression ◽  
Low Density

Receptor-mediated binding and metabolism of low-density lipoproteins (LDL) in cultured human vascular smooth-muscle cells and skin fibroblasts are altered by increased cellular cyclic AMP concentrations. However, the LDL receptor does not respond to changes in cyclic AMP concentration in a simple manner. The activation of adenylate cyclase with forskolin, or the addition of membrane-permeant cyclic AMP analogues, initially decreases the expression of the LDL receptor, but is followed by a substantial increase in receptor expression after 24 h. This increase does not occur in the presence of inhibitors of RNA or protein synthesis, and is due to doubling of the Bmax. of the LDL receptor, without alteration of its affinity for LDL. By contrast, elevation of cyclic AMP concentration by inhibition of phosphodiesterases results in decreased receptor expression throughout the 24 h period. These two response patterns are reproducible phenomena, consistently observed in low-passaged cells derived from seven unrelated individuals.

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