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PubMed1981

Mechanics and energetics of lengthening of active airway smooth muscle.

For smooth muscle in general there appears only one report dealing with force-velocity (FV) relationships of active muscle subjected to forcible elongation by application of loads (P) greater than its maximum isometric tetanic tension (Po); for airway smooth muscle (ASM) there is none. Since ASM may be subjected to increasing stretch during inspiration, the relationship is important and was therefore studied with canine tracheal smooth muscle (TSM) as a model. FV data for P less than Po could be fitted by Hill's hyperbolic equation. For P greater than Po, lengthening velocity was greater than predicted by the equation. However at equivalent velocities, the muscle during elongation could support a load three times greater than during shortening; in this it resembled skeletal muscle. From this it may be speculated that distension of the airway during inspiration would not be associated with mechanical instability. With reference to energy requirements of the elongating TSM it was shown, as has been for skeletal muscle, that the net rate of energy liberation (assessed by measuring tissue levels of adenosine triphosphate and creatine phosphate) in an elongating active muscle is less than that of a muscle contracting isometrically.

Adenosine Triphosphate↗
PubMed1995

Binding of A1 adenosine receptor ligand [3H]8-cyclopentyl-1,3-dipropylxanthine in coronary smooth muscle.

Vascular smooth muscle has been reported to contain the A1 subtype of adenosine receptors, but the existence of such receptor(s) in coronary smooth muscle has not been established. In the present study, the 3H-labeled A1-selective antagonist [3H]8-cyclopentyl-1,3-dipropylxanthine ([3H]DPCPX) was used to demonstrate the specific binding in porcine coronary artery smooth muscle membranes. The binding was saturable with a Bmax of 6.43 +/- 1.02 fmol/mg protein. Scatchard analysis of the binding data provided a single binding site with a Kd of 0.21 +/- 0.025 nmol/L. In the competition experiments, adenosine receptor agonists and antagonists showed the following order of potency (nmol/L): S-N6-(2-endonorbornyl)adenosine (S-ENBA) 0.11 = R(-)-N6-phenylisopropyladenosine 0.32 > DPCPX 3.2 = xanthine amine congener 2.4 = N6-cyclopentyladenosine 2.67 > 5'-(N-ethylcarboxamido)-adenosine 7.35 >> 2-[p-(2-carboxyethyl)-phenethyl-amino]-5'-(N-ethylcarboxamido)- adenosine 1000 > theophylline 83,000. This order of potency fits the criteria for the A1 adenosine receptor. S-ENBA, a highly selective A1 receptor agonist, was used to investigate the effect on isoproterenol-mediated vasorelaxation and cAMP accumulation. S-ENBA (0.1 to 10 nmol/L) dose-dependently shifted the isoproterenol-mediated (10(-8) to 10(-5) mol/L) vasorelaxation to the right in vascular rings. S-ENBA (10 nmol/L) inhibited the basal cAMP levels by 36% and attenuated the isoproterenol (10(-5) mol/L)-stimulated cAMP by 25% in the coronary rings. These inhibitory effects of S-ENBA on isoproterenol-mediated cAMP-accumulation and vasorelaxation were abolished by pertussis toxin (100 ng/mL, overnight) treatment of the arteries.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1999

Angiostatin binds to smooth muscle cells in the coronary artery and inhibits smooth muscle cell proliferation and migration In vitro.

Angiostatin is an inhibitor of angiogenesis that is known to reduce endothelial cell proliferation and consequently prevent the progression of tumor metastases. However, the modest effect of angiostatin on endothelial cell proliferation raises the possibility that angiostatin might exert its effects on other cells. To determine the cellular distribution of angiostatin binding in tissues with neovasculature (atherosclerotic coronary arteries), we developed a fusion protein consisting of placental alkaline phosphatase and the first 3 kringles of plasminogen. Angiostatin binding colocalized with smooth muscle cells and could be inhibited by a 50-fold molar excess of plasminogen and 10 mmol/L epsilon-amino-n-caproic acid. The fusion protein also bound to smooth muscle cells in culture. Angiostatin inhibited hepatocyte growth factor-induced proliferation and migration of smooth muscle cells, suggesting that they are a target for the antiangiogenic effect of angiostatin.

Alkaline Phosphatase↗
PubMed1991

Evidence for altered Na+/H+ antiport activity in cultured skeletal muscle cells and vascular smooth muscle cells from the spontaneously hypertensive rat.

1. Intracellular pH and Na+/H+ antiport activity were determined by a fluorimetric method in cultured skeletal muscle cells (myoblasts) and aortic vascular smooth muscle cells from spontaneously hypertensive and normotensive Wistar-Kyoto rats. 2. The intracellular pH was significantly more alkaline at three different extracellular pH values in both myoblasts and vascular smooth muscle cells from the spontaneously hypertensive rats than in those from the normotensive control rats. 3. A kinetic analysis of the Na+/H+ antiport activity in these cells showed that the raised activity in the spontaneously hypertensive rats was due to an increased maximal transport capacity in vascular smooth muscle cells and to an increase in the affinity of the antiport for internal H+ in the myoblasts. 4. When the extracellular pH was reduced in the skeletal muscle cells of both types of rat, the intracellular pH fell. However, in vascular smooth muscle cells, a reduction in the extracellular pH was not associated with a fall in the intracellular pH. This resistance of the intracellular pH to changes in the extracellular pH differentiates vascular smooth muscle cells from other cells that have been studied in this way.

Animals↗
PubMedDate not supplied

Cross talk between plasma membrane and sarcoplasmic reticulum in canine airway smooth muscle.

In smooth muscle, contractions under pharmacomechanical and electromechanical coupling mechanism control rely on mobilization of intracellular calcium and on calcium influx from the extracellular space, respectively. In airway smooth muscle, pharmacomechanical coupling seems to predominate. Even if extracellular calcium enters the cell during agonist stimulation, and contributes to the maintained plateau phase of a prolonged stimulation-induced contraction, it does not result from membrane depolarization and is not part of the electromechanical coupling mechanism. Pharmacomechanical and electromechanical coupling are most likely not independent processes: we present here an example of cross talk between plasma membrane and sarcoplasmic reticulum, which results in an almost complete switch in the E-C coupling process from pharmaco- to electromechanical mode in tracheal smooth muscle.

Animals↗
PubMed1982

Cholinergic and peptidergic receptors on isolated human antral smooth muscle cells.

Smooth muscle cells were isolated from segment so of human antrum obtained at operation. The presence, activity, and specificity of receptors to acetylcholine, the C-terminal octapeptide of cholecystokinin, methionine-enkephalin, and vasoactive intestinal peptide were examined. Muscarinic cholinergic receptors sensitive to low concentrations of atropine, cholecystokinin receptors sensitive to proglumide and dibutyryl cyclic guanosine monophosphate, enkephalin receptors sensitive to naloxone were demonstrated and found to mediate contraction. Vasoactive intestinal peptide receptors were demonstrated also and found to mediate relaxation. The stoichiometry and specificity of responses were closely similar to those previously found in isolated gastric smooth muscle cells of the guinea pig. The existence of high-affinity functional receptors on smooth muscle cells, together with the presence of the peptides in nerve terminals adjacent to these cells, makes it possible for these peptides to act as neurotransmitters.

Cholecystokinin↗
PubMed2000

The pathology of uterine smooth muscle tumors and mixed endometrial stromal-smooth muscle tumors: a selective review with emphasis on recent advances.

This review focuses on the pathology of uterine smooth muscle tumors (SMTs), with a particular emphasis on those studies published in the past 15 years that have expanded our knowledge of these tumors which still present diagnostic challenges for the pathologist. Leiomyoma variants, leiomyosarcoma, SMTs of low or uncertain malignant potential, epithelioid SMTs, SMTs with unusual growth patterns, and mixed endometrial stromal-SMTs are discussed.

Cell Nucleus↗
PubMed1991

Changes in Schultz-Dale reaction in sensitized canine tracheal smooth muscle.

Tracheal smooth muscles from adult dogs 17 to 20 months of age sensitized with ragweed pollen demonstrated a Schultz-Dale phenomenon in response to specific antigen challenge. Seventy percent of the sensitized tracheal smooth muscles developed a Schultz-Dale reaction that consisted only of a phasic response, and the remaining 30% developed a Schultz-Dale reaction that consisted of a phasic component followed by a discrete tonic component. All the Schultz-Dale reactions were mediated only by histamine. The triggering of presynaptic acetylcholine release by histamine during the Schultz-Dale reaction from tracheal smooth muscles of ragweed-pollen-sensitized puppies 6 to 8 months of age was not detected in sensitized adult dogs. Hyperresponsiveness to acetylcholine was detected in tissues from sensitized puppies but not from sensitized adult dogs. Maximal active tension obtained from the sensitized adult canine trachealis during the Schultz-Dale reaction was lower than that obtained from trachealis from sensitized puppies. Dose-response studies showed that sensitized tissues used in the present studies were hyperresponsive to histamine when compared with their nonsensitized control littermates. These results suggest that the nature of the Schultz-Dale response and the identity of the transmitters is age-dependent.

Acetylcholine↗
PubMed1987

Myosin light chain isoforms and their phosphorylation in arterial smooth muscle.

Arterial smooth muscle myosin contains nonphosphorylated and phosphorylated light chains that appear as 4 spots on two-dimensional, Coomassie blue-stained gel electrophoretograms at the 20,000-molecular weight level (referred to as spots 4 through 1 in order of decreasing isoelectric points). Anti-light chain recognizes the proteins in all 4 light chain spots. Complete dephosphorylation of light chain in muscle homogenate, by inhibiting myosin light chain kinase and by adding phosphatase, leads to 2 spots on two-dimensional gel electrophoretograms; both spots are visible on immunoblots. Stimulation (K+ or stretch) of smooth muscle results in increased light chain phosphorylation. Autoradiography of the gel electrophoretograms reveals that radioactive components are contained in spots 3, 2, 1, and in an additional spot with lower isoelectric point, referred to as spot 0. Phosphoamino acid analysis shows that spots 3 and 1 contain phosphoserine, whereas spots 2 and 0 contain phosphoserine and phosphothreonine. Two-dimensional phosphopeptide mapping of the trypsin-digested proteins from spots 3 and 1 shows predominantly 2 peptides; whereas from spots 2 and 0, it shows 5 peptides. Sodium dodecyl sulfate gel electrophoresis of the phosphopeptides obtained with Staphylococcus aureus V8 digestion gives identical maps for spots 3 and 2, which are different from the identical maps of spots 1 and 0. The results suggest that arterial smooth muscle myosin contains 2 nonphosphorylated 20,000-dalton light chain isoforms with different amino acid sequences and that each isoform can be mono- and diphosphorylated.

Animals↗
PubMed2001

Myosin thick filament lability induced by mechanical strain in airway smooth muscle.

Airway smooth muscle adapts to different lengths with functional changes that suggest plastic alterations in the filament lattice. To look for structural changes that might be associated with this plasticity, we studied the relationship between isometric force generation and myosin thick filament density in cell cross sections, measured by electron microscope, after length oscillations applied to the relaxed porcine trachealis muscle. Muscles were stimulated regularly for 12 s every 5 min. Between two stimulations, the muscles were submitted to repeated passive +/- 30% length changes. This caused tetanic force and thick-filament density to fall by 21 and 27%, respectively. However, in subsequent tetani, both force and filament density recovered to preoscillation levels. These findings indicate that thick filaments in airway smooth muscle are labile, depolymerization of the myosin filaments can be induced by mechanical strain, and repolymerization of the thick filaments underlies force recovery after the oscillation. This thick-filament lability would greatly facilitate plastic changes of lattice length and explain why airway smooth muscle is able to function over a large length range.

Animals↗
PubMed1981

Elastin formation in heterotopic transplants of isolated arterial smooth muscle cells.

Smooth muscle cells were isolated from the aorta of 5 day old rats by collagenase digestion and injected intramuscularly into animals of the same strain, where the cells reconstituted an elastic tissue with many similarities to that found in the media of the intact aortic wall. The transplants consisted of partly aligned smooth muscle cells surrounded by an extracellular matrix of microfibrils, elastic fibers, bundles of collagen fibrils, and small granules believed to represent proteoglycans. The production of extracellular matrix was much more efficient than in cultures of arterial smooth muscle cells. This cell transplantation system may be valuable in elucidating the mechanisms of normal growth and development of the arterial wall as well as the pathogenesis of various pathological processes.

Animals↗
PubMed2006

Shear stress induces endothelial transdifferentiation from mouse smooth muscle cells.

Smooth muscle cells (SMCs) under shear stress may alter their gene expression patterns to adapt to a new hemodynamic environment. Their plasticity may play an important role in vascular development, healing, and remodeling as well as vascular lesion formation under abnormal environmental conditions. A mouse vascular SMC line (P53LMACO1) cultured under shear stress significantly increased the mRNA levels of endothelial cell markers including Platelet-endothelial cell adhesion molecule-1 (PECAM-1), von Willebrand factor (vWF), and VE-cadherin, while significantly decreasing the mRNA levels of SMC markers including alpha-smooth muscle actin (alpha-SMA), calponin-1, smooth muscle myosin heavy chain (SMMHC), and transgelin as compared to static control cells. Protein levels of PECAM-1 and vWF were significantly increased, while protein levels of alpha-SMA were substantially decreased in the shear stress-cultured cells. In addition, shear stress-cultured cells showed an enhanced capability to form capillary-like structures on Matrigel. Thus, shear stress may promote endothelial cell transdifferentiation from SMCs.

Animals↗
PubMed1998

Regulation and tuning of smooth muscle myosin.

Smooth muscle myosin is regulated by phosphorylation of one of the two myosin light chains. This phosphorylation causes an unfolding of the myosin that allows it to interact with actin to produce force. The inactive state involves trapping the myosin in a conformation wherein the myosin heads interact with a segment of the myosin rod. Phosphorylation of the regulatory light chain weakens these interactions and allows the myosin to be activated. Smooth muscle myosin has a large movement of its light chain binding domain that is coupled to ADP release. This structural change may be necessary for the generation of "latch." Smooth muscle myosin has three different regions that vary to generate different isoforms: (1) an alternative insertion within the myosin head; (2) two possible essential light chains; and (3) an alternative tail at the end of the myosin rod. There is substantial evidence that the insertion in the myosin head increases the enzymatic activity of the myosin and leads to greater shortening velocity. The function of the other two variants is as yet unclear.

Actins↗
PubMed2003

Regulation of force in vascular smooth muscle.

Vascular smooth muscle contraction plays a defining role in the regulation and maintenance of blood pressure, and its deregulation is associated with many clinical syndromes including hypertension, coronary vasospasm and congestive heart failure. Over the past 20 years, there has been a growing understanding of the regulation of 20 kDa myosin light chain phosphorylation by myosin light chain kinase and myosin light chain phosphatase, the role of splice-variant isoforms of both the myosin heavy chain and the essential myosin light chain, as well as the signaling pathways involved in smooth muscle contraction under normal and pathophysiological conditions. This review will attempt to recapitulate the data in the field, primarily focusing on the contractile response of smooth muscle, and the molecular determinants responsible for the regulation of vascular tone.

Animals↗
PubMed1982

Dipyridamole: an antioxidant that promotes the proliferation of aorta smooth muscle cells.

Smooth muscle cells from guinea pig aorta were grown in tissue culture. Dipyridamole enhanced the proliferation of these cells in culture and dipyridamole overcame the inhibitory effect of arachidonic acid on cell proliferation. Dipyridamole and the antioxidant vitamin E both increased the cloning potential and the number of population doublings for smooth muscle cells in culture. Lipid peroxidation was measured in cultured cells with thiobarbituric acid. Dipyridamole, vitamin E and butylated hydroxytoluene inhibited lipid peroxidation both in cultures treated with media alone and in cultures treated with arachidonic acid. Dipyridamole enhanced PGI2 biosynthesis while vitamin E and butylated hydroxytoluene had no effect on PGI2 biosynthesis. These data show that cell proliferation is related to lipid peroxidation rather than PGI2 biosynthesis. Dipyridamole functions as an antioxidant that stimulates the proliferation of aorta smooth muscle cells.

Animals↗
PubMed1988

Expression of smooth muscle myosin in relation to growth kinetics of cultured aortic smooth muscle cells.

The goal of this study is to quantify smooth muscle myosin (SMM) expression at the level of the individual cell and to ascertain whether SMM expression in cultured aortic smooth muscle cells is related to definite growth phases, and whether the initial seeding density affects growth or SMM staining. Rabbit aortic smooth muscle cells (SMCs) were harvested by enzyme digestion of aortic tissue and plated at low (100 cells cm-2), medium (1000 cells cm-2), and high (10,000 cells cm-2) densities. Independent of seeding density, the lag phase lasted 2 to 3 days and, at all three densities, the growth rate during the logarithmic growth phase was almost the same. However, the time, the number of population doubling needed to reach the plateau phase and the cell number in the plateau were influenced by the initial seeding density. Immunofluorescence staining with anti-smooth muscle myosin (ASMM) revealed intensive staining of striated and filamentous patterns in all cells during the lag and early logarithmic growth phases. During the late logarithmic growth phase, two subpopulations of cells appeared, one showing a positive and the other no reaction with SMM antiserum. The lowest relative number of cells which showed positive reactions with SMM antiserum was observed toward the end of the logarithmic growth phase. During the plateau phase, the SMM-positive subpopulation increased, amounting to about 60% of the total number of cells, independent of the seeding density. In terms of absolute numbers, the number of SMM-positive cells increased over the course of 21 days by factors of 13, 72, and 342 for high, medium, and low seeded cultures, respectively. We conclude that a SMC subpopulation can divide without loss of SMM and that some, but not all, cells which lose their SMM may possibly regain it in the postconfluent state.

Animals↗
PubMed1990

Receptors on target cells. Receptors on airway smooth muscle.

Airway smooth muscle is a complex tissue that, in common with most other cell types, possesses a multitude of specific binding proteins that are coupled usually via guanine nucleotide regulation proteins to intracellular effector mechanisms. The development of sophisticated probes and biochemical approaches should allow an in-depth characterization of receptor subtypes, expression, regulation, and coupling to effector mechanisms that are activated as a consequence of ligand/receptor interaction. To date, most receptors in airway smooth muscle appear to be coupled via G proteins to these effector systems: PI turnover, adenylate cyclase, or phospholipase C. Qualitative and quantitative estimates of receptor proteins and the nature and efficiency of coupling to these effector mechanisms need to be linked to physiologic function and the regulation of airway smooth muscle response in health and disease.

Adrenergic Fibers↗
PubMed1991

Effect of TNF on triacylglycerol in cultured vascular smooth muscle cells.

Smooth muscle cells (SMC) isolated from bovine aorta or human saphenous vein were cultured and used to study the putative effect of recombinant human tumor necrosis factor (TNF) on lipid metabolism in vascular cells. Addition of TNF to the culture medium for 24-48 h resulted in an increase of [3H]oleic acid uptake and esterification into lipids. The effect could be seen already with 0.3 ng/ml and was maximal with 30 ng/ml. The effect of TNF was mainly on the incorporation of [3H]oleic acid into triacylglycerol which increased by 140% in the bovine cells. There was also a significant increase in [3H]cholesteryl ester. In the human SMC there was a 40% increase in [3H]oleic acid into total lipids, while the rise in [3H]triacylglycerol ranged between 60-90%. TNF did not modulate cellular triacyglycerol synthesis in cultured mouse peritoneal macrophages. Since TNF was shown to be synthesized and secreted not only by macrophages but also by smooth muscle cells, it could play an autocrine role in lipid metabolism during development of atherosclerotic lesions. The cellular population of the lesions, i.e., predominance of macrophages or smooth muscle cells, could determine the relative proportion of triacylglycerol accumulation.

Animals↗