smooth/proline

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Cyclic strain stimulates L-proline transport in vascular smooth muscle cells.

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BACKGROUND The increase in vessel wall strain in hypertension contributes to arterial remodeling by stimulating vascular smooth muscle cell (SMC) proliferation and collagen synthesis. Because L-proline is essential for the synthesis of collagen and cell growth, we examined whether cyclic strain

Adrenomedullin stimulates proline-rich tyrosine kinase 2 in vascular smooth muscle cells.

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A novel vasodilator peptide, adrenomedullin (AM) stimulates extracellular signal-regulated kinase (ERK) 1/2 via yet uncharacterized 120 kDa tyrosine kinase(s) in rat vascular smooth muscle cells (VSMC). In the present study, we have examined whether the AM-activated tyrosine kinase is proline-rich

Pharmacological studies of kinins in venous smooth muscles.

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The myotropic effects of bradykinin (BK) and other kinins in two isolated veins, the rabbit jugular and the guinea pig anterior mesenteric, have been studied. The effects of degradation on the biological activities of these compounds and the receptor types mediating their myotropic effects have been

Allylamine-induced phenotypic modulation of aortic smooth muscle cells.

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Subchronic exposure of Sprague-Dawley rats for 20 days to allylamine resulted in a modulation of phenotypic expression of smooth muscle cells in vitro as characterized by alterations in cell morphology, ultrastructure, contractile function and synthetic/proliferative capabilities. Smooth muscle

Endothelial cell effect on smooth muscle cell collagen synthesis.

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Extracellular matrix (ECM) constitutes the bulk of mature intimal hyperplastic lesions. To determine if endothelial cells (ECs) inhibit smooth muscle cell (SMC) collagen synthesis, bovine aortic SMCs were cultured on plastic semipermeable membranes either alone or opposite ECs. SMCs were pulsed with

Carbon monoxide modulates alpha-smooth muscle actin and small proline rich-1a expression in fibrosis.

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Carbon monoxide (CO) is a biologically active molecule produced in the body by the stress-inducible enzyme, heme oxygenase. We have previously shown that CO suppresses fibrosis in a murine bleomycin model. To investigate the mechanisms by which CO opposes fibrogenesis, we performed gene expression

CF airway smooth muscle transcriptome reveals a role for PYK2.

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Abnormal airway smooth muscle function can contribute to cystic fibrosis (CF) airway disease. We previously found that airway smooth muscle from newborn CF pigs had increased basal tone, an increased bronchodilator response, and abnormal calcium handling. Since CF pigs lack airway infection and

Bladder smooth muscle cells in culture: I. Identification and characterization.

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This report documents the growth and culture characteristics of human and fetal bovine bladder smooth muscle cells in vitro. Bladder smooth muscle cell strains have been identified by their spindle shaped morphology, noncontact inhibited growth characteristics and the expression of smooth muscle

Effect of physical forces on bladder smooth muscle and urothelium.

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Abnormalities in bladder physiology may be due to obstruction (pressure) and/or neurological impairment. Clinically they can result in an increase in connective tissue and a decrease in bladder compliance. To study the effects of physical forces on the bladder without the influence of the nerves we

A(2B) receptors mediate antimitogenesis in vascular smooth muscle cells.

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Adenosine inhibits growth of vascular smooth muscle cells. The goals of this study were to determine which adenosine receptor subtype mediates the antimitogenic effects of adenosine and to investigate the signal transduction mechanisms involved. In rat aortic vascular smooth muscle cells,

The synthesis of connective tissue protein in smooth muscle cells.

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The synthesis of elastin by smooth muscle cells was clearly demonstrated by amino acid analyses and the presence of lysine-derived crosslinks. The values obtained were compatible with those found in amorphous elastin isolated from rabbit aortic tissue. Collagen synthesis by these same cells was

Inhibitory effect of dehydrozingerone on vascular smooth muscle cell function.

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OBJECTIVE Growth factor and oxidative stress-mediated migration and proliferation of vascular smooth muscle cells (VSMCs) play a key role in the pathogenesis of atherosclerosis. The objective of this study was to assess the ability of dehydrozingerone, a structural analog of curcumin, to inhibit

Dipeptidyl(amino)peptidase IV and post proline cleaving enzyme in cultured endothelial and smooth muscle cells.

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Dipeptidyl(amino)peptidase IV (DAP IV; EC 3.4.14.5) and post proline cleaving enzyme (PPCE; EC 3.4.21.26) can convert or degrade vasoactive peptides and have been identified in isolated vessels. The present study examined the cellular (endothelial/smooth muscle) localization of vascular DAP IV and

Collagen production by human smooth muscle cells isolated during intestinal organogenesis.

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The extracellular matrix influences organogenesis by modulating cell behavior. In humans, collagen is the major matrix constituent of the adult intestinal wall and is synthesized by smooth muscle cells. The objective of the current study was to examine collagen production by fetal human intestinal

Angiotensin II stimulates collagen synthesis in cultured vascular smooth muscle cells.

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The aim of the present study was to investigate whether angiotensin II, by increasing extracellular matrix synthesis, contributed to the vascular wall thickening observed in hypertension. Thus, we examined the direct effects of angiotensin II on collagen and fibronectin synthesis in cultured rat

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