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PubMed1995

Smooth muscle cells and atherosclerosis.

The role of smooth muscle cells in atherogenesis involves cell proliferation and accretion of cholesteryl ester. Smooth muscle cell proliferation, controlled by growth factors produced locally, contributes to progression of atheroma and to restenosis after percutaneous transluminal coronary angioplasty. Accretion of cholesteryl ester in smooth muscle cells is mediated by factors secreted by macrophages. Induction of the scavenger receptor in smooth muscle cells may promote the transformation to foam cells. Novel approaches to combat restenosis include gene transfer into smooth muscle cells using different vectors.

Angioplasty, Balloon, Coronary↗
PubMedDate not supplied

Clinical update of smooth muscle tumors of the uterus.

Smooth muscle tumors of the uterus represent a spectrum of diseases that range from benign leiomyoma to malignant leiomyosarcoma. The leiomyoma is the most common of these neoplasms. Clinically, it is important to fully understand the differences in clinical presentation, biologic behavior, and management for patients with benign leiomyoma, smooth muscle tumors of uncertain malignant potential, and leiomyosarcoma. The goal of this review is to present the most recent information about common smooth muscle tumors of the uterus including their etiology, histopathology, radiographic and clinical presentations, and available treatment options.

Endoscopy↗
PubMed2005

CD40 and OX40 ligand are increased on stimulated asthmatic airway smooth muscle.

BACKGROUND: Severe, persistent asthma is characterized by airway smooth muscle hyperplasia, inflammatory cell infiltration into the smooth muscle, and increased expression of many cytokines, including IL-4, IL-13, IL-1beta, and TNF-alpha. These cytokines have the potential to alter the expression of surface receptors such as CD40 and OX40 ligand on the airway smooth muscle cell. OBJECTIVE: To examine whether cytokines alter expression of CD40 and OX40 ligand on airway smooth muscle cells and identify any differences in response between asthmatic and nonasthmatic airway smooth muscle cells. METHODS: We used flow cytometry and immunohistochemistry to detect CD40 and OX40 ligand on airway smooth muscle cells cultured in the presence of TNF-alpha, IL-1beta, IL-4, or IL-13. Prostaglandin E 2 levels were assessed by ELISA. RESULTS: TNF-alpha increased expression of both CD40 and OX40 ligand on both asthmatic and nonasthmatic airway smooth muscle cells. The level of expression was significantly greater on the asthmatic cells. IL-1beta alone had no effect, but it attenuated the TNF-induced expression of both CD40 and OX40 ligand. The mechanism of inhibition was COX-dependent for CD40 and was COX-independent but cyclic AMP-dependent for OX40 ligand. IL-4 and IL-13 had no effect. CONCLUSION: Our study has demonstrated that TNF-alpha and IL-1beta have the potential to modulate differentially the interactions between cells present in the inflamed airways of a patient with asthma and therefore to contribute to the regulation of airway inflammation and remodeling.

Adult↗
PubMed1994

Smooth muscle phosphatases: structure, regulation, and function.

Smooth muscle contraction is regulated primarily by the reversible phosphorylation of myosin by myosin light chain kinase. Secondary mechanisms that might modulate contractility are phosphorylation-dephosphorylation of myosin light chain kinase and thin-filament proteins, caldesmon and calponin. Purification of several protein phosphatases that are active toward myosin light chains and (or) myosin and heavy meromyosin from smooth muscles has been reported. All the cytosolic turkey gizzard smooth muscle phosphatases, termed SMP-I, -II, -III, and -IV, dephosphorylate myosin light chains rapidly, but only SMP-III and -IV are active toward myosin and heavy meromyosin, suggesting that SMP-III and -IV might be directly involved in the relaxation of smooth muscle. SMP-III and -IV exhibit properties typical of type 1 protein phosphatases following tryptic digestion. These enzymes appear to share structural similarity with myofibrillar phosphatase PP1M. Purified calponin phosphatase and caldesmon phosphatase from chicken gizzards are structurally and immunologically identical with SMP-I, a type 2A protein phosphatase. SMP-I dephosphorylates calponin faster than it does caldesmon, and has much higher activity toward these substrates than SMP-II, -III, and -IV. Thus, one role for SMP-I might be to regulate the activities of caldesmon and calponin. Since SMP-I is active toward myosin light chain kinase, it might also modulate this enzyme.

Animals↗
PubMed1999

In vivo human brachial artery elastic mechanics: effects of smooth muscle relaxation.

BACKGROUND: The effects of smooth muscle relaxation on arterial wall mechanics are controversial. We used a new, in vivo, noninvasive technique to measure brachial artery wall mechanics under baseline conditions and following smooth muscle relaxation with nitroglycerin (NTG). METHODS AND RESULTS: Eight healthy, normal subjects (6 male, 2 female; age 30+/-3.1 years) participated in the study. The nondominant brachial artery was imaged through a water-filled blood pressure cuff using an external ultrasound wall-tracking system at baseline and following 0.4 mg sublingual NTG. Simultaneous radial artery pressure waveforms were recorded by tonometry. Transmural pressure (TP) was reduced by increasing water pressure in the cuff. Brachial artery area, unstressed area, compliance, stress, strain, incremental elastic modulus (Einc), and pulse wave velocity (PWV) were measured over a TP range from 0 to 100 mm Hg. Baseline area versus TP curves generated 30 minutes apart were not significantly different. NTG significantly shifted area versus TP (P<0.0001) and compliance versus TP (P<0.001) curves upward, whereas the Einc versus TP (P<0.05) and PWV versus TP (P<0. 01) curves were shifted downward. NTG also significantly shifted stress versus strain (P<0.01) and Einc versus strain (P<0.01) curves to the right. CONCLUSIONS: We conclude that brachial artery elastic mechanics can be reproducibly measured over a wide range of TP and smooth muscle tone using a new noninvasive ultrasound technique. Smooth muscle relaxation with NTG increases isobaric compliance and decreases isobaric Einc and PWV in the human brachial artery.

Adult↗
PubMed1994

Functional evidence for a glibenclamide-sensitive K+ channel in rat ileal smooth muscle.

The motor activity of gastrointestinal smooth muscle is closely related to the membrane potential. Controlling the membrane potential via modulation of K+ channels is essential for the action of neurotransmitters on smooth muscle. In the present study the effect of the K+ channel activator, lemakalim, on longitudinal smooth muscle of the rat ileum was investigated. Segments of rat ileum were stimulated by the muscarinic receptor agonist, carbachol (10(-6) M). Lemakalim (10(-10) to 3 x 10(-5) M) induced a dose-dependent inhibition of the carbachol-induced contraction. This inhibitory effect of lemakalim was not modified by neural blockade with tetrodotoxin (10(-6) M, n = 9). Glibenclamide (10(-7) to 10(-5) M), a specific blocker of ATP-dependent K+ channels antagonized dose dependently the relaxant effect of lemakalim (IC50: 3.4 x 10(-6) M, n = 11, P < 0.001). In contrast, apamin (10(-7) M, n = 9, n.s.) and charybdotoxin (10(-7) M, n = 9, n.s.), specific blockers of Ca2+-dependent K+ channels and the non-specific K+ channel blocker, tetraethylammonium (10(-4) to 10(-1) M), had no influence on the inhibitory effect of lemakalim. Contractions induced by the Ca2+ channel activator, Bay-K-8644, were completely inhibited by lemakalim (10(-5) M, n = 12). This inhibitory effect was also selectively antagonized by glibenclamide (10(-5) M). Potential non-adrenergic non-cholinergic (NANC) inhibitory mediators like ATP, nitric oxide (NO) or neurotensin showed no sensitivity to glibenclamide. These functional data indicate that the relaxant effect of lemakalim is due to a specific activation of glibenclamide-sensitive K+ channels, which in turn can modulate the activity of dihydropyridine-sensitive (voltage-dependent) Ca2+ channels. A physiological or pathophysiological role of the glibenclamide-sensitive K+ channels in intestinal smooth muscle is discussed; however, they seem not to be involved in the effect of the NANC inhibitory mediators tested.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1986

Stimulation of aortic smooth muscle cell mitogenesis by serotonin.

Bovine aortic smooth muscle cells in vitro responded to 1 nM to 10 microM serotonin with increased incorporation of [3H]thymidine into DNA. The mitogenic effect of serotonin was half-maximal at 80 nM and maximal above 1 microM. At a concentration of 1 microM, serotonin stimulated smooth muscle cell mitogenesis to the same extent as human platelet-derived growth factor (PDGF) at 12 ng/ml. Tryptamine was approximately 1/10th as potent as serotonin as a mitogen for smooth muscle cells. Other indoles that are structurally related to serotonin (D- and L-tryptophan, 5-hydroxy-L-tryptophan, N-acetyl-5-hydroxytryptamine, melatonin, 5-hydroxyindoleacetic acid, and 5-hydroxytryptophol) and quipazine were inactive. The stimulatory effect of serotonin on smooth muscle cell DNA synthesis required prolonged (20-24 hr) exposure to the agonist and was attenuated in the presence of serotonin D receptor antagonists. When smooth muscle cells were incubated with submaximal concentrations of serotonin and PDGF, synergistic rather than additive mitogenic responses were observed. These data indicate that serotonin has a significant mitogenic effect on smooth muscle cells in vitro, which appears to be mediated by specific plasma membrane receptors.

Animals↗
PubMed2005

Modeling the oscillation dynamics of activated airway smooth muscle strips.

When strips of activated airway smooth muscle are stretched cyclically, they exhibit force-length loops that vary substantially in both position and shape with the amplitude and frequency of the stretch. This behavior has recently been ascribed to a dynamic interaction between the imposed stretch and the number of actin-myosin interactions in the muscle. However, it is well known that the passive rheological properties of smooth muscle have a major influence on its mechanical properties. We therefore hypothesized that these rheological properties play a significant role in the force-length dynamics of activated smooth muscle. To test the plausibility of this hypothesis, we developed a model of the smooth muscle strip consisting of a force generator in series with an elastic component. Realistic steady-state force-length loops are predicted by the model when the force generator obeys a hyperbolic force-velocity relationship, the series elastic component is highly nonlinear, and both elastic stiffness and force generation are adjusted so that peak loop force equals isometric force. We conclude that the dynamic behavior of airway smooth muscle can be ascribed in large part to an interaction between connective tissue rheology and the force-velocity behavior of contractile proteins.

Animals↗
PubMedDate not supplied

Does nitric oxide regulate smooth muscle cell proliferation? A critical appraisal.

Smooth muscle proliferation is involved in the pathogenesis of atherosclerosis, restenosis after angioplasty and vein graft failure due to neointimal hyperplasia. Nitric oxide (NO) inhibits smooth muscle cell growth in vitro and experimental neointimal hyperplasia in vivo, suggesting a role for NO as a regulator of smooth muscle cell proliferation. NO is also involved in the control of numerous other vascular functions including platelet and inflammatory cell adhesion, vascular reactivity and endothelial permeability. This review critically examines the experimental and clinical evidence that supports a role for NO as a modulator of smooth muscle cell proliferation, with an emphasis on the multiple mechanisms by which NO acts on vascular lesions.

Animals↗
PubMed1997

Smooth muscle myosin light chain kinase is transiently expressed in skeletal muscle during embryogenesis and muscle regeneration both in vivo and in vitro.

By using a polyclonal antibody raised against smooth muscle Myosin Light Chain Kinase of adult chicken we show that the 135 kDa smooth muscle Myosin Light Chain Kinase isoform is present in neonatal and regenerating rat skeletal muscle, as well as in adult atrial myocardium. No reaction was evident in adult skeletal muscle fibres. In neonatal and in early regenerating muscle smooth muscle Myosin Light Chain Kinase is associated with embryonic myosin as revealed by their co-presence in muscle fibres. Experiments in vitro show the same results in myotubes. In atrial myocardium there is a patchy positivity in certain group of myocytes. Immunoblotting experiments show in muscle cell cultures, in neonatal and in regenerating skeletal muscle a protein band with electrophoretic mobility corresponding to that of smooth muscle Myosin Light Chain Kinase. These results suggest that the expression of smooth muscle Myosin Light Chain Kinase is not fully tissue-specific and that regulation of the contractile machinery could be different during myogenesis and in adulthood, in relation to the peculiar dynamic characteristics of developing muscles.

Animals↗
PubMed1993

Chimeric regulatory light chains as probes of smooth muscle myosin function.

Functional domains of the smooth muscle regulatory light chain (LC) were identified from the assembly and motor properties of smooth muscle myosin containing chimeric LCs, in which the N- and C-terminal halves of the smooth and skeletal LCs were interchanged. A C-terminal domain was also expressed. The affinity of these LCs for the smooth muscle myosin heavy chain (HC) is: wild-type LC > N-skeletal/C-smooth > N-smooth/C-skeletal approximately skeletal LC >> C-terminal domain. The C-terminal half of the LC thus contains an isoform-specific HC binding site, but the two halves of the LC must interact for tight binding. Smooth muscle myosin containing chimeric or skeletal LCs can no longer assume the folded monomeric conformation, suggesting that control of assembly involves both halves of the LC. Dephosphorylation/phosphorylation of the N-skeletal/C-smooth chimera nonetheless regulates the ability of smooth muscle myosin to move actin. Myosin containing phosphorylated N-smooth/C-skeletal or skeletal LCs, in contrast, is locked in the "off" state. Interactions between the stronger binding C-terminal domain of the LC and the HC are therefore primarily responsible for the regulatory capabilities of this subunit. Localization of the regulatory LC at the head/rod junction by electron microscopy establishes that phosphorylation-induced changes must be transmitted over 10 nm within the head for product release to be enhanced.

Amino Acid Sequence↗
PubMed1993

Critical intracellular Ca2+ concentration for all-or-none Ca2+ spiking in single smooth muscle cells.

Neurotransmitters induce contractions of smooth muscle cells initially by mobilizing Ca2+ from intracellular Ca2+ stores through inositol 1,4,5-trisphosphate (InsP3) receptors. Here we studied roles of the molecules involved in Ca2+ mobilization in single smooth muscle cells. A slow rise in cytoplasmic Ca2+ ([Ca2+]i) in agonist-stimulated smooth muscle cells was followed by a wave of rapid regenerative Ca2+ release as the local [Ca2+]i reached a critical concentration of approximately 160 nM. Neither feedback regulation of phospholipase C nor caffeine-sensitive Ca(2+)-induced Ca2+ release was found to be required in the regenerative Ca2+ release. These results indicate that Ca(2+)-dependent feedback control of InsP3-induced Ca2+ release plays a dominant role in the generation of the regenerative Ca2+ release. The resulting Ca2+ release in a whole cell was an all-or-none event, i.e. constant peak [Ca2+]i was attained with agonist concentrations above the threshold value. This finding suggests a possible digital mode involved in the neural control of smooth muscle contraction.

Animals↗
PubMed2006

Roles of CaM kinase II and phospholamban in SNP-induced relaxation of murine gastric fundus smooth muscles.

The mechanisms by which nitric oxide (NO) relaxes smooth muscles are unclear. The NO donor sodium nitroprusside (SNP) has been reported to increase the Ca2+ release frequency (Ca2+ sparks) through ryanodine receptors (RyRs) and activate spontaneous transient outward currents (STOCs), resulting in smooth muscle relaxation. Our findings that caffeine relaxes and hyperpolarizes murine gastric fundus smooth muscles and increases phospholamban (PLB) phosphorylation by Ca2+/calmodulin (CaM)-dependent protein kinase II (CaM kinase II) suggest that PLB phosphorylation by CaM kinase II participates in smooth muscle relaxation by increasing sarcoplasmic reticulum (SR) Ca2+ uptake and the frequencies of SR Ca2+ release events and STOCs. Thus, in the present study, we investigated the roles of CaM kinase II and PLB in SNP-induced relaxation of murine gastric fundus smooth muscles. SNP hyperpolarized and relaxed gastric fundus circular smooth muscles and activated CaM kinase II. SNP-induced CaM kinase II activation was prevented by KN-93. Ryanodine, tetracaine, 2-aminoethoxydiphenylborate, and cyclopiazonic acid inhibited SNP-induced fundus smooth muscle relaxation and CaM kinase II activation. The Ca2+-activated K+ channel blockers iberiotoxin and apamin inhibited SNP-induced hyperpolarization and relaxation. The soluble guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo-[4,3-alpha]quinoxalin-1-one inhibited SNP-induced relaxation and CaM kinase II activation. The membrane-permeable cGMP analog 8-bromo-cGMP relaxed gastric fundus smooth muscles and activated CaM kinase II. SNP increased phosphorylation of PLB at Ser16 and Thr17. Thr17 phosphorylation of PLB was inhibited by cyclopiazonic acid and KN-93. Ser16 and Thr17 phosphorylation of PLB was sensitive to 1H-[1,2,4]oxadiazolo-[4,3-alpha]quinoxalin-1-one. These results demonstrate a novel pathway linking the NO-soluble guanylyl cyclase-cGMP pathway, SR Ca2+ release, PLB, and CaM kinase II to relaxation in gastric fundus smooth muscles.

Animals↗
PubMed1992

Identification and characterization of developmentally regulated genes in vascular smooth muscle cells.

We wish to understand the process of smooth muscle cell (SMC) proliferation and maturation during late fetal development and have examined some of the molecular changes associated with blood vessel maturation in late gestational and early neonatal life. By differential screening of a fetal aortic smooth muscle cDNA library, we identified a gene (F-31) that was developmentally regulated in aortic smooth muscle. The F-31 gene encodes a 2.3-kb RNA that was highly expressed in fetal aortic smooth muscle (25-day gestation), was lower in newborns, and was undetectable in the aortic smooth muscle of 4-week-old animals. F-31 was also highly expressed in fetal muscle, esophagus, heart, liver, lung, and placenta; its expression was lower in skin, kidney, and brain. By contrast, the expression of F-31 was low or undetectable in the corresponding tissue of adult animals. DNA sequence analysis of cDNAs encoding F-31 and data base comparison revealed a 73% homology with a previously identified, developmentally regulated gene called H19. We also found that insulin-like growth factor II (IGF-II) expression was developmentally regulated in smooth muscle. However, unlike F-31, expression of IGF-II was undetectable in the aortic smooth muscle of newborn animals. Analysis of the mRNA level of several genes that encode cytoskeletal proteins in neonatal, newborn, and adult smooth muscle indicates that total actin mRNA level, alpha-smooth muscle actin, and alpha-tropomyosin mRNA levels were similar between the late gestational period and 4 weeks after birth.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1990

Endothelial cell matrices modulate smooth muscle cell growth, contractile phenotype and sensitivity to heparin.

Whereas vascular smooth muscle cell-extracellular matrix interactions have been intensively studied, our knowledge regarding the role that matrix plays in regulating the growth state and contractile phenotype of vessel wall cells is fragmentary. Of particular interest has been the demonstrable ability of (1) heparin to selectively inhibit vascular smooth muscle cell growth in vitro; (2) aortic endothelial cells to produce a heparin-like inhibitor of vascular smooth muscle cells, and (3) heparin to reverse smooth muscle cell proliferation in arteries that have been experimentally denuded of their endothelium. Recent work from our laboratory indicates that the endothelial cell synthesized extracellular matrix alters growth rate and heparin sensitivity of vascular smooth muscle cells. Whereas endothelial cell synthesized matrices that contain collagen and fibronectin promote smooth muscle cell growth, matrices containing heparan sulfate proteoglycan selectively inhibit identical smooth muscle cell populations. Similarly, these heparan sulfate enriched matrices lower smooth muscle sensitivity to heparin and positively influence the endothelial cells' ability to produce the heparin-like inhibitor of vascular smooth muscle cell growth. In an effort to understand the mechanism mediating heparin's effects on smooth muscle cell proliferation and contractile phenotype, we have analyzed the effects of heparin on vascular smooth muscle cell shape and actin isoform expression using doses of heparin previously shown to be growth inhibitory. The results of our studies indicate that heparin alters smooth muscle cell shape and cytoskeletal organization, suggesting that heparin's growth inhibitory action may be related to its effects on cell shape. Additionally, the permissive effects that different endothelial matrices exert on vascular smooth muscle may selectively predispose specific subpopulations of arterial cells towards a proliferating phenotype, one associated with the genesis of atherosclerosis.

Animals↗
PubMed1969

Ultrastructural studies on the contractile mechanism of smooth muscle.

Fresh taenia coli and chicken gizzard smooth muscle were studied in the contracted and relaxed states. Thick and thin filaments were observed in certain (but not all) cells fixed in contraction. Relaxed smooth muscle contained only thin filaments. Several other morphological differences were observed between contracted and relaxed smooth muscle. The nuclear chromatin is clumped in contraction and evenly dispersed in the relaxed state. The sarcolemma is more highly vesiculated in contraction than in relaxation. In contraction, the sarcoplasm also appears more electron opaque. Over-all morphological differences between cells fixed in isometric and in unloaded contraction were also noticeable. The results suggest a sliding filament mechanism of smooth muscle contraction; however, in smooth muscle, unlike striated muscle, the thick filaments appear to be in a highly labile condition in the contractile process. The relation between contraction and a possible change in pH is also discussed.

Animals↗
PubMed2006

Synergistic roles of platelet-derived growth factor-BB and interleukin-1beta in phenotypic modulation of human aortic smooth muscle cells.

The phenotype of smooth muscle cells (SMCs) plays an important role in vascular function in health and disease. We investigated the mechanism of modulation of SMC phenotype (from contractile to synthetic) induced by the synergistic action of a growth factor (platelet-derived growth factor, PDGF-BB) and a cytokine (interleukin, IL-1beta). Human aortic SMCs grown on polymerized collagen showed high expression levels of contractile markers (smooth muscle alpha-actin, myosin heavy chain, and calponin). These levels were not significantly affected by PDGF-BB and IL-1beta individually, but decreased markedly after the combined usage of PDGF-BB and IL-1beta. PDGF/IL-1beta costimulation also induced a sustained phosphorylation of Akt and p70 ribosomal S6 kinase (p70S6K). The effects of PDGF/IL-1beta costimulation on contractile marker expression and Akt and p70S6K phosphorylation were blocked by the phosphatidylinositol 3-kinase inhibitors wortmannin and LY294002 and by adenovirus expressing a dominant-negative Akt, and they were mimicked by constitutively active Akt. PDGF-BB/IL-1beta induced a sustained phosphorylation of PDGF receptor (PDGFR)-beta and its association with IL-1 receptor (IL-1R1). Such activation and association of receptors were blocked by a PDGFR-beta neutralizing antibody (AF385), an IL-1R1 antagonist (IL-1ra), as well as a specific inhibitor of PDGFR-beta phosphorylation (AG1295); these agents also eliminated the PDGF-BB/IL-1beta-induced signaling and phenotypic modulation. PDGF-BB/IL-1beta inhibited the polymerized collagen-induced serum response factor DNA binding activity in the nucleus, and this effect was mediated by the PDGFR-beta/IL-1R1 association and phosphatidylinositol 3-kinase/Akt/p70S6K pathway. Our findings provide insights into the mechanism of SMC phenotypic modulation from contractile to synthetic, e.g., in atherosclerosis.

Aorta↗
PubMed2000

Cyclic GMP-dependent protein kinase expression in coronary arterial smooth muscle in response to balloon catheter injury.

Arterial smooth muscle cells undergo phenotypic and proliferative changes in response to balloon catheter injury. Nitric oxide (NO) and cGMP have been implicated in the inhibition of vascular smooth muscle cell proliferation and phenotypic modulation in cultured-cell studies. We have examined the expression of the major cGMP receptor protein in smooth muscle, cGMP-dependent protein kinase I (PKG), in response to balloon catheter injury in the swine coronary artery. On injury, there was a transient decrease in the expression of PKG in neointimal smooth muscle cells when compared with medial smooth muscle cells. The decrease in PKG expression was observed in the population of proliferating cells expressing the extracellular matrix protein osteopontin but not in cells present in the uninjured portion of the media. Coincident with the suppression of PKG expression in neointimal cells after injury, there was a marked increase in the expression of type II NO synthase (inducible NOS [iNOS], NOS-II) in the neointimal cells. These results suggest that PKG expression is transiently reduced in response to injury in the population of coronary arterial smooth muscle cells that are actively proliferating and producing extracellular matrix proteins. The reduction in PKG expression is also correlated temporally with increases in inflammatory activity in the injured vessels as assessed by iNOS expression. Coupled with our current knowledge regarding the role of PKG in the regulation of cultured cell phenotypes, these results imply that PKG may also regulate phenotypic modulation of vascular smooth muscle cells in vivo as well.

Angioplasty, Balloon↗