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PubMed1987

The calcium antagonist nisoldipine and the calmodulin antagonist W-7 synergistically inhibit initiation of DNA synthesis in cultured arterial smooth muscle cells.

Cultured arterial smooth muscle cells go through a transition from a contractile to a synthetic phenotype. Morphologically, the transition includes a reduction in size of the myofilament bundles and the formation of an extensive rough endoplasmic reticulum and a large Golgi complex. Functionally, it leads to loss of contractility, onset of cellular proliferation, and secretion of extracellular matrix components. This change in differentiated characteristics under in vitro conditions has attracted attention because of its resemblance to the modification of the smooth muscle cells that occurs in vivo during atherogenesis. Here, transmission electron microscopy and [3H]-thymidine autoradiography were used to study the role of calcium ions in the control of phenotypic properties and growth of cultivated rat aortic smooth muscle cells. The calcium antagonist nisoldipine was found to lack distinct effect on the structural reorganization of the cells, but showed a moderate prohibitory effect on the start of DNA synthesis early in primary culture. In growth-arrested secondary cultures, nisoldipine inhibited induction of DNA synthesis by serum or platelet-derived growth factor (PDGF). The agent's effect was inversely related to the concentration of calcium ions in the extracellular medium and was partially counteracted by the calcium agonist BAY K 8644. In contrast, W-7, an antagonist of the calcium-binding protein calmodulin, potentiated the effect of nisoldipine and, at higher concentrations, inhibited induction of DNA synthesis in itself. The results suggest that the mitogenic stimulation of arterial smooth muscle cells involves a flux of calcium ions through the plasma membrane and requires participation of calmodulin.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2006

[Isolation and physiological characterization of mesenteric arterial smooth muscle cells].

Vascular smooth muscle cells (VSMCs) are crucial for studying the mechanism and regulation of vasogenic response, but so far no ideal method has been reported for their isolation. We established a VMSC isolation method based on two-step digestion, with which a large population of single smooth muscle cells could be obtained. After cell isolation, the potassium current, cytosolic calcium concentration, reactivity to caffeine were measured, and the results demonstrated that the cells were highly viable and exhibited reactivity to the vascular constrictor to meet various needs in experimental research.

Animals↗
PubMed1999

Troglitazone inhibits alpha1-adrenoceptor-induced DNA synthesis in vascular smooth muscle cells.

While vascular smooth muscle cell proliferation is important in hypertension, relatively little is known about the contribution of catecholamines. Novel insulin sensitizing agents, thiazolidinediones, have been demonstrated to inhibit angiotensin II-, basic fibroblast growth factor (FGF)-induced growth of vascular smooth muscle cells. We hypothesize that these agents might also inhibit the effect of the stimulation of alpha1-adrenoreceptors on the proliferation of vascular smooth muscle cells. Troglitazone (1-20 microM), a member of the thiazolidinediones, significantly inhibited the stimulation of alpha1-adrenoreceptor-induced DNA synthesis, c-fos induction and mitogen-activated protein (MAP)-kinase activation. This effect was associated with inhibition by troglitazone of the transactivation of the serum response element (SRE), which regulates c-fos expression. Inhibition of c-fos induction by troglitazone appeared to occur via blockade of the upstream of MAP kinase activation in vascular smooth muscle cells. At this dose, troglitazone inhibited the ternary complex factor (TCF)-dependent activation, which is regulated by MAP kinase activation, but did not inhibit the TCF-independent SRE activation. Besides, the degree of the inhibitory effect of troglitazone on MAP kinase activation, DNA synthesis, c-fos expression differs. This may show that troglitazone work on multiple sites. These results suggest that troglitazone is a potent inhibitor of vascular smooth muscle cells proliferation through the downregulation of c-fos expression and may be a useful agent for prevention of atherosclerosis which is a result of hypertension.

Animals↗
PubMed1987

Stretch-induced membrane depolarization in ferret trachealis smooth muscle cells.

We determined the effects of increasing the length of the ferret trachealis muscle on smooth muscle membrane potentials recorded on successive impalements by microelectrodes. The preparation included the paratracheal ganglion nerve plexus as well as trachealis muscle. With sustained increases in muscle length over the range 0.5-0.8 to 1.2 maximal length (Lmax), depolarization occurred, which was related to the amplitude of the length increase. Membrane depolarizations were also evoked after stretching to lengths approximately 1.1 Lmax and returning to the control length. Stretch-induced membrane depolarizations developed after the stretch maneuver was complete; were slowly reversible; were not influenced by tetrodotoxin or atropine; were related to stretch rather than to maintained increase in muscle length; were not transmitted to adjacent nonstretched segments of the trachea; and were often associated with slow waves which appear to be secondary to membrane depolarization rather than stretch per se.

Animals↗
PubMed1994

Simultaneous activation of adenylyl cyclase and protein kinase C induces production of nitric oxide by vascular smooth muscle cells.

Rat aortic smooth muscle cells produced large quantities of nitric oxide (NO) after exposure to interleukin-1 beta, and this was depressed in the presence of the protein kinase C inhibitor bisindolylmaleimide. Intracellular cAMP levels were elevated mildly in cytokine-treated smooth muscle cells, and the presence of forskolin enhanced both the cAMP levels and NO production. Inhibition of GTP:cyclohydrolase I by 2,4-diamino-6-hydroxypyrimidine attenuated NO production by interleukin-1 beta-treated cells. GTP:cyclohydrolase is the regulatory enzyme for de novo tetrahydrobiopterin synthesis, and the latter is a required cofactor for NO synthase activity. Treatment of smooth muscle cells with forskolin induced GTP:cyclohydrolase mRNA expression, and simultaneous treatment of cells with forskolin and phorbol esters elicited NO production. Angiotensin II and arginine-vasopressin, acknowledged agonists for protein kinase C, elicited production of NO by forskolin-treated smooth muscle cells. These observations confirm the importance of GTP:cyclohydrolase activity for NO production by cultured smooth muscle cells and implicate both adenylyl cyclase and protein kinase C in this process.

Adenylyl Cyclases↗
PubMed2002

On the mechanisms whereby temperature affects excitation-contraction coupling in smooth muscle.

Moderate cooling of smooth muscle can modulate force production and may contribute to pathophysiological conditions, but the mechanisms underlying its effects are poorly understood. Interestingly, cooling increases force in rat ureter, but decreases it in guinea pigs. Therefore, this study used ureteric smooth muscle as a model system to elucidate the mechanisms of the effects of cooling on excitation-contraction coupling. Simultaneous recordings of force, intracellular [Ca(2+)], and electrical activity were made in intact ureter and ionic currents measured in isolated cells. The increase in force amplitude in rat ureter with cooling was found to be due to a significant increase in the duration of the Ca(2+) transient. This in turn was due to a marked prolongation of the action potential. In guinea pigs, both these parameters were much less affected by cooling. Examination of membrane currents revealed that differences in ion channel contribution to the action potential underlie these differences. In particular, cooling potentiated Ca(2+)-activated Cl(-) currents, which are present in rat but not guinea pig ureteric smooth muscle, and prolonged the plateau of the action potential and Ca(2+) entry. The force-Ca(2+) relationship revealed that the increased duration of the Ca(2+) transient was sufficient in the rat, but not in the guinea pig, to overcome kinetic lags produced in both species by cooling and potentiate force. Ca(2+) entry and release processes were largely temperature-insensitive, but the rate of relaxation was very temperature-sensitive. Effects of cooling on myosin light chain phosphatase, confirmed in experiments using calyculin A, appear to be the predominant mechanisms affecting relaxation. Thus, smooth muscle is diverse in its response to temperature, even when experimental variables, such as the mode of stimulation, are removed. Although the biochemical and mechanical events accompanying contraction are likely to be affected in similar ways by temperature, differences in electrical events lead to subsequent differences in these processes between smooth muscles.

Action Potentials↗
PubMed1986

Tracheal smooth muscle.

Contraction of tracheal smooth muscle requires the binding of Ca2+ to calmodulin, which then binds to and activates MLCK. The Ca2+-calmodulin-MLCK complex catalyzes the phosphorylation of myosin, which causes contraction by stimulating actin-activated Mg2+-ATPase activity of myosin. Myosin phosphorylation appears to be a transient event that is responsible for a high velocity of shortening. The mechanism responsible for maintenance of isometric force is unknown, although a second Ca2+-dependent mechanism with a greater sensitivity to Ca2+ than the activation of MLCK has been hypothesized. Force would be maintained through the slow cycling of nonphosphorylated cross-bridges or a small population of phosphorylated cross-bridges. Tracheal smooth muscle utilizes both extracellular and intracellular pools of Ca2+ for contraction. Moreover, the membrane channels through which extracellular Ca2+ passes have been subdivided into potential-dependent channels (PDCs) and receptor-operated channels (ROCs) independent of membrane potential. The relative extent to which extracellular and intracellular sources of Ca2+ as well as PDCs and ROCs are utilized depends on the agonist used for contraction, its concentration, and the type and location of the smooth muscle being investigated. Calcium antagonists such as verapamil and nifedipine, which reportedly block PDCs but not ROCs, are much better inhibitors of tracheal smooth muscle contractions induced by serotonin than those induced by acetylcholine, histamine, and leukotriene D4, indicating an effect of these latter three agents on ROCs. Relaxation of tracheal smooth muscle following stimulation of beta-adrenergic receptors most likely results from an increase in cAMP that stimulates a cAMP-dependent protein kinase to catalyze a protein phosphorylation that leads to relaxation by decreasing the intracellular concentration of Ca2+. The primary mechanisms whereby cAMP is thought to reduce intracellular Ca2+ to effect relaxation include: activation of a calmodulin-sensitive Ca2+ ATPase in the plasma and sarcoplasmic reticulum membranes, and extrusion of Ca2+ by a Na+-Ca2+ exchange mechanism coupled to Na+-K+-ATPase in the cell membrane. A more controversial mechanism for relaxation that bypasses Ca2+ might involve the dephosphorylation of myosin. Leukotrienes are released by various stimuli, including immunologic challenge, and have been considered as important mediators of bronchoconstriction in allergic asthma.(ABSTRACT TRUNCATED AT 400 WORDS)

Biomechanical Phenomena↗
PubMed1996

Molecular cloning and characterization of SmLIM, a developmentally regulated LIM protein preferentially expressed in aortic smooth muscle cells.

Differentiated, quiescent vascular smooth muscle cells assume a dedifferentiated, proliferative phenotype in response to injury, one of the hallmarks of arteriosclerosis. Members of the LIM family of zinc-finger proteins are important in the differentiation of various cells including striated muscle. We describe here the molecular cloning and characterization of a developmentally regulated smooth muscle LIM protein, SmLIM, that is expressed preferentially in the rat aorta. This 194-amino acid protein has two LIM domains, and comparisons of rat SmLIM with its mouse and human homologues reveal high levels of amino acid sequence conservation (100 and 99%, respectively). SmLIM is a nuclear protein and maps to human chromosome 3. SmLIM mRNA expression was high in aorta but not in striated muscle and low in other smooth muscle tissues such as intestine and uterus. In contrast with arterial tissue, SmLIM mRNA was barely detectable in venous tissue. The presence of SmLIM expression within aortic smooth muscle cells was confirmed by in situ hybridization. In vitro, SmLIM mRNA levels decreased by 80% in response to platelet-derived growth factor-BB in rat aortic smooth muscle cells. In vivo, SmLIM mRNA decreased by 60% in response to vessel wall injury during periods of maximal smooth muscle cell proliferation. The down-regulation of SmLIM by phenotypic change in vascular smooth muscle cells suggests that it may be involved in their growth and differentiation.

Amino Acid Sequence↗
PubMed1979

Smooth muscle autoantibodies and autoantigens.

Smooth muscle autoantibody (SMA) was first found in the sera of patients with chronic active hepatitis and subsequently in the sera of patients with other autoimmune liver diseases, viral infections, certain cancers, heroin addicts and female infertility. SMA from patients with chronic active hepatitis reacts with many muscle and 'non-muscle' tissues while SMA from patients with other diseases usually reacts only with smooth muscle. These differences in immunofluorescent staining reactions suggest that SMA is a heterogeneous group of autoantibodies reactive with different smooth muscle autoantigens. As further evidence for this are findings that broad-reacting SMA can be absorbed out by actin, whereas autoantibodies reactive only with smooth muscle cannot, and that different SMAs give different immunofluorescent staining patterns using fibroblasts in tissue culture. Such staining patterns correspond to reactivity with either microfilaments, microtubules or intermediate filaments, ubiquitous cytoplasmic structures which make up the 'cytoskeleton'. Autoantibodies to actin-like microfilaments appear specific for chronic active hepatitis, autoantibodies to microtubules occur in infectious mononucleosis whereas autoantibodies to intermediate filaments occur in infectious hepatitis, chickenpox, measles and mumps. Predictably, future studies will show that presence of SMA with specificities for other proteins in the three types of cytoplasmic filaments, and given more information on antigenicity of the proteins and pathogenicity of the corresponding autoantibodies.

Actins↗
PubMed1997

G-protein regulation of an L-type calcium channel current in canine jejunal circular smooth muscle.

Calcium entry into smooth muscle cells is essential to maintain contractility. In canine jejunal circular smooth muscle cells the predominant calcium entry pathway is through L-type calcium channels. The aim of this study was to determine the G-protein regulation of L-type calcium channel current (ICaL) in isolated canine jejunal circular smooth muscle cells. Barium (80 mM) was used as the charge carrier. GTP-gamma S and GTP increased maximal inward current from 118.7 +/- 12 pA to 227.5 +/- 21.5 pA (n = 8) and 174.6 +/- 10.1 pA (n = 6) respectively. The increase in inward current was blocked by nifedipine suggesting it was through L-type calcium channels. Pertussis toxin did not alter baseline ICaL while cholera toxin increased ICaL from 125 +/- 19 pA in controls (n = 6) to 347 +/- 30 pA (n = 4). Staurosporine inhibited the increase in current evoked by GTP-gamma S and calyculin further increased ICaL over the increase evoked by GTP-gamma S. The results suggest that cholera toxin sensitive G-proteins activate L-type calcium channels in isolated canine jejunal circular smooth muscle cells through protein phosphorylation.

Animals↗
PubMed1984

Static contraction of hindlimb muscles in cats reflexly relaxes tracheal smooth muscle.

Static contraction of skeletal muscle is associated with increased ventilation. Although chemical stimulation of afferents from skeletal muscle causes relaxation of tracheal smooth muscle, it is not known if skeletal muscle contraction also causes tracheal relaxation. Therefore, in 10 chloralose-anesthetized cats, I examined the hemodynamic and tracheal smooth muscle responses to hindlimb skeletal muscle contraction induced by stimulating the L7 and S1 ventral roots. Isometric tension was measured in the transverse cervical trachea. During contraction average gastrocnemius tension increased from 0.7 +/- 0.1 to 4.9 +/- 0.6 kg, blood pressure and heart rate increased from 100 +/- 8 to 128 +/- 9 mmHg and from 192 +/- 11 to 202 +/- 13 beats/min, respectively, whereas tracheal tension decreased from 19.7 +/- 0.4 to 17.5 +/- 0.7 g (all P less than 0.02). There were significant (P less than 0.01) linear correlations between change in tracheal tension and maximal developed tension (r = -0.65), tension time (r = -0.68), and average developed tension (r = -0.76). Transection of the L7 and S1 dorsal roots in six cats reduced the tracheal relaxation associated with muscle contraction (pre: 19.9 +/- 0.3 to 17.5 +/- 0.3 g vs. post: 20.3 +/- 0.4 to 20.3 +/- 0.6 g) while average developed gastrocnemius muscle tension was not altered (pre: 1.1 +/- 0.1 to 6.4 +/- 1.1 kg vs. post: 1.2 +/- 0.2 to 6.8 +/- 1.2 kg). Thus static contraction of hindlimb muscles in cats reflexly lowers tracheal tension. This response is related to muscle mass and total tension generated by the contracting skeletal muscle.

Animals↗
PubMed1996

Markers of airway smooth muscle cell phenotype.

Airway smooth muscle plays a principal role in the pathogenesis of asthma. Primary cultures are being used to investigate airway myocyte proliferation and cellular pathways regulating contraction. Airway smooth muscle cells (SMC) modulate from a contractile to a noncontractile phenotype in culture, but no systematic study of the concomitant changes in expression of cytocontractile and cytoskeletal proteins has been reported. We measured temporal changes in protein marker expression of canine tracheal SMC in primary culture, using specific antibodies and cDNA probes. Immunoblot analysis revealed that when cells became proliferative after 5 days of culture, the content of smooth muscle myosin heavy chain (sm-MHC), calponin, sm-alpha-actin, and desmin diminished by > 75%; myosin light chain kinase, h-caldesmon, and beta-tropomyosin had also decreased significantly (P < 0.05). Northern blots revealed that mRNA levels for sm-MHC and sm-alpha-actin were also significantly reduced in proliferative SMC. Conversely, immunoblotting demonstrated the content of non-muscle myosin heavy chain, l-caldesmon, vimentin, alpha/beta-protein kinase C (PKC), and CD44 homing cellular adhesion molecule (HCAM) increased one- to sixfold as cells became proliferative. The content of sm-MHC and sm-alpha-actin protein increased after confluence, suggesting that cultured airway SMC are capable of phenotypic plasticity. Marker protein contents were also compared, by immunoblot assay, between SMC dissociated from trachealis or pulmonary arterial media. Cytocontractile protein content was higher in the trachea, which shortens faster than the pulmonary artery. The identification of these markers provides tools for assessing the phenotype of airway SMC in culture and the airways of asthmatic patients.

Animals↗
PubMed2000

The formation of the chick ileal muscle layers as revealed by alpha-smooth muscle actin immunohistochemistry.

The genesis of intestinal smooth muscle layers was immunohistochemically investigated by use of an antibody to alpha-smooth muscle actin (alpha-SMA) in the developing chick ileum. Myoblast cells positive for alpha-SMA were already found in the presumptive circular muscle layer on E 8.5. On E 11.5 radially oriented muscle fibers were protruded from the outermost layer of the developing circular musculature and then formed a tuft-like aggregates. These radial muscle bundles were bent into an L-shape. The long distal extension of muscle bundles run parallel to the long axis of the ileal loop and developed into the longitudinal muscle layer. The obliquely oriented muscle fibers, locating at the intermuscular space of the muscularis propria, probably are to be considered a remnant of the short extension of radial muscle bundles. The muscularis mucosae was formed by the processes equivalent to the genesis of longitudinal muscle layer. On E 14.5 centripetally oriented muscle fibers emerged from the innermost layer of circular musculature. The long distal extension of centripetal fibers lay along the inner surface of developing circular musculature. On E 19.5 the longitudinal muscle layer of the muscularis mucosae was newly formed by separating from the circular musculature. The villous myoblast cells initially developed from the innermost layer of the muscularis mucosae on E 18.5, and were widely distributed in the lamina propria mucosae on E 20.5. Temporal and chronological pattern in expression of alpha-SMA was observed during the development of the chick intestinal smooth muscle. By E 14.5 the entire layer of the muscularis propria was intensely immunostained for alpha-SMA, but from E 15.5 onward the staining intensity gradually began to decrease from the outer half of the circular musculature. Finally, the immunoreactivity was localized in the inner layer of circular muscle and the longitudinal muscle layer. A possible functional role of this inner layer of circular muscle is discussed.

Actins↗
PubMed1980

[Immunohistochemical detection of antibodies against smooth muscle (author's transl)].

Smooth muscles antibodies are heterogeneous. Their fluorescent staining patterns and their antigens are not exactly known. The author's own experiences are based on 170 smooth muscle antibodies, which were tested by means of indirect immunofluorescence for their binding to rat stomach, liver, kidney, heart, and bovine skeletal muscle, further to human lymphocytes (only 10 cases were tested). 123 different fluorescent patterns and 21 combinations of various organs were found. Few unusual patterns were demonstrated. There was evidence that antibodies with individuum specificity exist, e.g. antibodies reacted only with the muscularis mucosae of the stomach. Possibilities of errors were discussed shortly. Smooth muscle antibodies reacting with stomach, liver, kidney (especially glomerular mesangium), and heart were more frequent in liver diseases than in non liver diseases (ratio about 4 : 1). Antibodies reacted with smooth, heart, and skeletal muscle were most anti-skeletal antibodies cross-reacted with smooth muscle.

Animals↗