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PubMed1972

Role of muscarinic cholinergic receptors in regulation of guanosine 3':5'-cyclic monophosphate content in mammalian brain, heart muscle, and intestinal smooth muscle.

Effects of acetylcholine and of agents that mimic or block its physiological actions have been studied upon concentrations of guanosine 3':5'-cyclic monophosphate (cyclic GMP) and adenosine 3':5'-cyclic monophosphate (cyclic AMP) in slices of mammalian cerebral cortex, heart ventricle, and ileum. Acetylcholine, and cholinomimetic agents with a predominantly muscarinic action, such as methacholine, bethanechol, and pilocarpine, induced an increase in the concentration of cyclic GMP, accompanied by no change or a slight decrease in the concentration of cyclic AMP, in all three tissues studied. Tetramethylammonium, a cholinomimetic agent with a predominantly nicotinic action, on the other hand, did not significantly alter concentrations of either cyclic GMP or cyclic AMP. The increase in the tissue content of cyclic GMP induced by acetylcholine and its muscarinic analogs was antagonized by atropine, a muscarinic blocking agent, but not by hexamethonium, a nicotinic blocking agent. These and other results suggest the generalization that the interaction of acetylcholine with muscarinic receptors, but not with nicotinic receptors, causes an increase in the concentration of cyclic GMP. The data are compatible with the hypothesis that cyclic GMP may mediate the muscarinic actions of acetylcholine. The antagonistic actions of cholinergic and adrenergic agents on the physiology of contraction of intestinal smooth muscle and of cardiac muscle are reflected in, and may result from, antagonistic actions of these compounds on the levels of both cyclic GMP and cyclic AMP in these tissues.

Acetylcholine↗
PubMed1990

Okadaic acid uncouples myosin light chain phosphorylation and tension in smooth muscle.

Tracheal smooth muscle precontracted with carbachol relaxes upon the addition of 3 microM okadaic acid. Although cytosolic Ca2+ concentrations decrease, myosin light chain remains highly phosphorylated (50%). In smooth muscle treated with carbachol alone or carbachol plus okadaic acid 32P is incorporated into a single peptide on myosin light chain which corresponds to the site phosphorylated by myosin light chain kinase. Treatment with okadaic acid alone does not result in myosin light chain phosphorylation or tension development. These results suggest that a cellular mechanism other than myosin light chain phosphorylation can regulate contractile tension.

Animals↗
PubMed2003

Isolation of bone marrow stromal cell-derived smooth muscle cells by a human SM22alpha promoter: in vitro differentiation of putative smooth muscle progenitor cells of bone marrow.

BACKGROUND: Bone marrow stromal cells (BMSCs) have many characteristics of mesenchymal stem cells that can differentiate into smooth muscle cells (SMCs). However, there have been few studies closely following the cell development of smooth muscle lineage among BMSCs. METHODS AND RESULTS: To investigate the possible existence of a cell population committed to the SMC lineage among bone marrow adhesion cells, we tried to detect and follow the in vitro differentiation of such a cell type by using a promoter-sorting method with a human SM22alpha promoter (-480 bp)/green fluorescent protein (GFP) construct. The construct was transfected to adhesion cells that appeared 5 days after the seeding of mononuclear cells from bone marrow. GFP was first detectable 5 days after the transfection in a cell population [Ad(G) cells], which expressed PDGF-beta but neither mature (calponin) nor immature (SMemb) SMC-specific proteins at that time. However, the cells were eventually grown into individual clones that expressed SMC-specific proteins (alpha-smooth muscle actin, calponin, and SM-1), suggesting that Ad(G) cells have partly at least progenitor properties. Because early studies have reported that PDGF-beta signaling plays pivotal roles in the differentiation of mesenchymal smooth muscle progenitor cells, Ad(G) cells might be putative mesenchymal smooth muscle progenitors expressing PDGF-beta. CONCLUSIONS: We demonstrated the presence of a cell population fated to become SMCs and followed their differentiation into SMCs among BMSCs.

Animals↗
PubMed1995

Mechanical strain increases contractile enzyme activity in cultured airway smooth muscle cells.

Smooth muscle hypertrophy is often found in tissue subjected to abnormal physical stress. To determine if physical stress (strain) per se could increase the contractile potential of airway smooth muscle (ASM), we compared cultured ASM cells subjected to strain to control cells (no strain) for rates of 1) myosin light chain kinase (MLCK)-mediated myosin light chain (LC20) phosphorylation, 2) actin-activated myosin ATPase, and 3) myosin light chain phosphatase-mediated myosin dephosphorylation. Lysates from strained cells showed increases in both LC20 phosphorylation activity and actomyosin ATPase activity but decreased rates of phosphatase-dependent myosin dephosphorylation. The increased LC20 phosphorylation activity and ATPase activity of the strained cells were accompanied by increases in cellular content of MLCK and myosin, respectively, compared with control. Because the cultured ASM cells exposed to strain expressed higher MLCK activity and actomyosin ATPase activity but lower myosin light chain phosphatase activity, these data suggest that physical stress in part determines ASM potential for contractile state.

Animals↗
PubMed2006

Spontaneously tonic smooth muscle has characteristically higher levels of RhoA/ROK compared with the phasic smooth muscle.

The internal anal sphincter (IAS) tone is important for the rectoanal continence. The RhoA/Rho kinase (ROK) pathway has been associated with the agonist-induced sustained contraction of the smooth muscle, but its role in the spontaneously tonic smooth muscle is not known. Present studies compared expression of different components of the RhoA/ROK pathway between the IAS (a truly tonic SM), the rectal smooth muscle (RSM) (a mixture of phasic and tonic), and anococcygeus smooth muscle (ASM) (a purely phasic SM) of rat. RT-PCR and Western blot analyses were performed to determine RhoA, ROCK-II, CPI-17, MYPT1, and myosin light-chain 20 (MLC20). Phosphorylated CPI-17 at threonine-38 residue (p(Thr38)-CPI-17), MYPT1 at threonine-696 residue (p(Thr696)-MYPT1), and MLC20 at threonine-18/serine-19 residues (p(Thr18/Ser19)-MLC20) were also determined in the basal state and after pretreatment with the ROK inhibitor Y 27632. In addition, we compared the effect of Y 27632 on the basal isometric tension and ROK activity in the IAS vs. the RSM. Our data show the highest levels of RhoA, ROCK-II, CPI-17, MLC20, and of phospho-MYPT1, -CPI-17, and -MLC20 in the IAS followed by in the RSM and ASM. Conversely, MYPT1 levels were lowest in the IAS and highest in the ASM. In the IAS, Y 27632 caused a concentration-dependent decrease in the basal tone, levels of phospho-MYPT1, -CPI-17, and -MLC20, and ROK activity. We conclude that RhoA/ROK plays a critical role in the basal tone in the IAS by the inhibition of MLC phosphatase via the phosphorylation of MYPT1 and CPI-17.

Amides↗
PubMed1994

Angiotensin type 1 receptors mediate smooth muscle proliferation and endothelin biosynthesis in rat vascular smooth muscle.

Angiotensin II (AII) has the potential to promote vascular smooth muscle (VSM) hypertrophy and hyperplasia; however, the mechanisms involved in AII stimulation of VSM growth are not fully understood. The AII receptor subtypes in VSM responsible for several biological events leading to cell proliferation have been evaluated. All-induced mitogenesis in explants of rat VSM cells was antagonized by the angiotensin type 1 (AT1)-selective receptor antagonists SK&F 108566 (IC50 = 5.3 +/- 0.96 nM) and DuP 753 (IC50 = 3.5 +/- 0.97 nM), but not by AT2 receptor antagonists. AII-stimulated endothelin (ET)-1 gene expression was antagonized by SK&F 108566 (50% at 1 microM), but not by selective AT2 receptor antagonists. Similarly, AII stimulated the release of immunoreactive ET (irET) from cultured VSM cells that was antagonized by 1 microM SK&F 108566 (72%) and DuP 753 (66%), but not by AT2 receptor antagonists. AII and growth factors that stimulated the release of irET down-regulated the number of ET receptor binding sites. AII (1-100 nM) markedly (6- to 10-fold) stimulated mitogen-activated protein kinase, an enzyme believed to be involved in the pathway for cell proliferation, and this stimulation was blocked (50-75%) by SK&F 108566 (1 nM-1 microM). Phosphoramidon (50 microM) inhibited (60%) both AII-induced irET release and cell proliferation. These data demonstrate that AII-mediated VSM growth is via AT1 receptors, and suggest that AII-induced ET production may contribute to the proliferative response in these cells.

Acrylates↗
PubMed1997

Expression and function of recombinant endothelial NO synthase in coronary artery smooth muscle cells.

Smooth muscle cells (SMCs) play a key role in the pathogenesis of vascular diseases. The objectives of this study were to determine whether transfer of recombinant endothelial nitric oxide synthase (eNOS) gene to porcine coronary artery smooth muscle cell (CSMCs) would result in expression of a functional enzyme and to assess the effect of expression of eNOS on cell proliferation. CSMCs were transduced in vitro with adenoviral vectors encoding cDNA for eNOS (AdeNOS) and beta-galactosidase (Ad beta Gal). In contrast to Ad beta Gal- or sham-transduced cells, CSMCs transduced with AdeNOS stained positive with the NADPH-diaphorase stain, acquired calcium-dependent NOS activity (measured by the conversion of [3H]L-arginine to [3H]L-citrulline), had increasing cyclic 3',5' cGMP levels with increasing concentrations of the vector, and produced increased amounts of nitrite. cGMP production by AdeNOS-transduced cells was augmented by increasing intracellular levels of the eNOS cofactor tetrahydrobiopterin. CSMCs transduced with AdeNOS showed diminished serum-stimulated DNA synthesis as measured by thymidine uptake. Cell proliferation was diminished in AdeNOS-transduced CSMCs as assessed by cell counts 3 and 6 days after serum stimulation of quiescent CSMCs. The present study demonstrates that adenovirus-mediated gene transfer of eNOS to CSMCs results in the expression of a functional enzyme whose activity can be augmented by increasing intracellular levels of tetrahydrobiopterin. Expression of recombinant eNOS in CSMCs results in inhibition of serum-stimulated DNA synthesis and cell proliferation. These findings imply that eNOS gene transfer to SMCs may be a unique mode of increasing local NO production in the arterial wall.

Adenoviridae↗
PubMed1995

Mechanisms for the mechanical plasticity of tracheal smooth muscle.

In smooth muscle tissues, the relationship between muscle or cell length and active force can be modulated by altering the cell or tissue length during stimulation. Mechanisms for this mechanical plasticity were investigated by measuring muscle stiffness during isometric contractions in which contractile force was graded by changing stimulus intensity or muscle length. Stiffness was significantly higher in contracted than in resting muscles at comparable forces; however, the relationship between stiffness and force during force development was curvilinear and independent of muscle length and stimulus intensity. This suggests that muscle stiffness during force development reflects properties of cellular components other than cross bridges which contribute to the series elasticity only during activation. During the tonic phase of isometric contraction, muscle stiffness increased while force remained constant. A step decrease in the length of a contracted muscle resulted in a high level of stiffness relative to force during isometric force redevelopment following the length step. We propose that the arrangement of the cytoskeleton can adjust to changes in the conformation of resting smooth muscle cells but that the organization of the cytoskeleton becomes more fixed upon contractile activation and is modulated very slowly during a sustained contraction. This may provide a mechanism for optimizing force development to the physical conformation of the cell at the time of activation.

Animals↗
PubMed2004

Bcl-2 receptor expression in patients with uterine smooth muscle tumors: an immunohistochemical analysis comparing leiomyoma, uterine smooth muscle tumor of uncertain malignant potential, and leiomyosarcoma.

OBJECTIVE: Bcl-2 protein is an apoptosis-inhibiting gene product that prevents the normal course of apoptotic cell death in a variety of cells. Additionally, bcl-2 can promote cell replication by reducing the requirement for growth factors. This protein seems, therefore, to play an important role in the growth of tumors. Our aim was to investigate the different expression of bcl-2 in uterine leiomyomas, smooth muscle tumors of uncertain malignant potential (STUMP), and leiomyosarcomas (LMS). Furthermore, the correlation between bcl-2 expression and various clinicopathologic parameters in leiomyosarcomas was assessed to evaluate its prognostic value. METHODS: This study included 26 cases of leiomyoma, 22 cases of STUMP, and 21 cases of LMS of the uterus. Bcl-2 expression was investigated by immunohistochemistry from paraffin-embedded tissue. The immunohistochemical findings were compared and correlated with different clinicopathologic parameters. Clinical information, including follow-up data, was obtained from the database of the Department of Gynecology and Obstetrics. RESULTS: Bcl-2 was present in 12 of 21 LMS, eight of 22 STUMP, and 20 of 25 leiomyomas. Significant differences regarding the frequency of bcl-2 expression and the staining intensity were observed between LMS and leiomyoma as well as between STUMP and leiomyoma (P <.05) but not between LMS and STUMP (P >.05). Regarding the outcome of uterine LMS, patients with bcl-2 positive tumors showed less vascular space involvement and longer overall survival (P <.05). CONCLUSION: Bcl-2 was expressed more frequently and more strongly in leiomyomas compared with LMS and STUMP. Regarding the outcome of uterine LMS, patients with bcl-2-positive tumors showed less vascular space involvement and longer overall survival. The stronger bcl-2 expression in benign leiomyomas and the better clinical outcome of bcl-2-positive LMS indicate that this protein seems to act as a good prognostic factor. Further studies including larger numbers of patients are necessary to establish bcl-2 as a routine marker for improved prognosis in malignant uterine smooth muscle tumors.

Adult↗
PubMed1992

Elements of the smooth muscle alpha-actin promoter required in cis for transcriptional activation in smooth muscle. Evidence for cell type-specific regulation.

To assess the role of cis-acting elements within the smooth muscle alpha-actin gene in smooth muscle cells (SMC), we transfected chicken smooth muscle alpha-actin promoter-chloramphenicol acetyltransferase gene fusion plasmids into SMC derived from rat and chicken aortas. In marked contrast to effects in chicken skeletal myoblasts and fibroblasts, p122CAT (positions -122 to +19), containing two conserved CArG elements, elicited a modest increase in chloramphenicol acetyltransferase reporter activity in chicken SMC. Addition of upstream sequences between -122 and -151 (p151CAT) increased activity in adult chicken SMC. Addition of sequence between positions -151 and -257 (p257CAT) resulted in a 7-fold increase in chloramphenicol acetyltransferase activity over that of p151CAT in rat SMC, but not in chicken SMC. A genomic clone encoding the rat smooth muscle alpha-actin gene was isolated, and the 5'-flanking region was partially characterized. Comparison of primary sequence between rat and chicken promoters showed a conserved E box motif at position -214 in the chicken gene and at position -213 in the rat gene. Results of these studies demonstrate that regions upstream of the conserved CArG elements exert potent regulatory effects on transcription and that SMC require different cis-acting elements than other cell types to transcriptionally regulate this gene.

Actins↗
PubMed1985

The influence of antiplatelet drugs on injury-stimulated migration of cultured smooth muscle cells.

Smooth muscle cell (SMC) migration, one of the early events in arteriosclerotic lesion formation in vivo, can be triggered by balloon catheter injury. This accelerated migration persists when aortic explants are grown in tissue culture. Under low serum conditions (0.1% fetal bovine serum) virtually no smooth muscle cell migration occurs out of explants from sham operated control animals, while over 70% of explants from balloon injured rats show SMC migration. Since platelets are thought to contribute to SMC proliferation and migration, we tested the effect of different antiplatelet drugs (sulfinpyrazone, aspirin, dipyridamole, and a combination of the last two) on balloon injury stimulated SMC migration. One week after onset of drug treatment balloon catheterization was performed and SMC migration from aortic explants was assessed 4 days later in vitro. The time and number of explants showing SMC migration was recorded daily over 8 days. Sulfinpyrazone reduced stimulated SMC migration most effectively, followed by the combination of aspirin and dipyridamole, while aspirin or dipyridamole alone had no significant effect on stimulated SMC migration. Using this technique we were able to single out SMC migration and analyze the effect of antiplatelet drugs on this early step in arteriosclerotic lesion formation.

Animals↗
PubMed2005

The proteome and secretome of human arterial smooth muscle cells.

Smooth muscle cells (SMCs) play a crucial role in cardiovascular disorders. A differential proteomic approach should help to elucidate SMC dysfunctions involved in these diseases. With this goal in mind, we plotted the first 2-dimensional (2-D) maps of the proteome and secretome of human arterial smooth muscle cell (ASMC). Intracellular and secreted proteins were extracted from a primary culture of SMCs obtained from patients undergoing coronary artery bypass surgery (n = 11) and separated by 2-dimensional gel electrophoresis. Silver-stained gels were analyzed using Progenesis software. A high level of between-gel reproducibility was obtained, allowing us to generate two protein patterns specific to the ASMC proteome and secretome, respectively. A total of 121 and 40 distinct intracellular and secreted polypeptide spots, corresponding to 83 and 18 different proteins, respectively, were identified by matrix-assisted laser desorption/ionization mass spectrometry. The 2-D reference maps and database resulting from this study confirm that SMCs are involved in a wide range of biological functions. They could constitute a useful tool for a wide range of investigators involved in vascular biology, allowing them to investigate SMC protein changes associated with cardiovascular disorders or environmental stimuli.

Cells, Cultured↗
PubMed1993

The mechanism for the activation of latent TGF-beta during co-culture of endothelial cells and smooth muscle cells: cell-type specific targeting of latent TGF-beta to smooth muscle cells.

Transforming growth factor-beta (TGF-beta) is secreted in a latent form and activated during co-culture of endothelial cells and smooth muscle cells. Plasmin located on the surface of endothelial cells is required for the activation of latent TGF-beta (LTGF-beta) during co-culture, and the targeting of LTGF-beta to the cellular surface is requisite for its activation. In the present study, the cellular targeting of LTGF-beta was examined. We detected the specific binding of 125I-large LTGF-beta 1 isolated from human platelets to smooth muscle cells but not to endothelial cells. A mAb against the latency-associated peptide (LAP) of large LTGF-beta 1 complex, which blocked the binding of 125I-large LTGF-beta 1 to smooth muscle cells, inhibited the activation of LTGF-beta during co-culture. The binding of 125I-large LTGF-beta 1 could not be competed either by mannose-6-phosphate (300 microM) or by the synthetic peptide Arg-Gly-Asp-Ser (300 micrograms/ml). These results indicate that the targeting of LTGF-beta to smooth muscle cells is required for the activation of LTGF-beta during co-culture of endothelial cells and smooth muscle cells. The targeting of LTGF-beta to smooth muscle cells is mediated by LAP, and the domain of LAP responsible for the targeting to smooth muscle cells may not be related to mannose-6-phosphate or an Arg-Gly-Asp sequence, both of which have been previously proposed as candidates for the cellular binding domains within LAP.

Amino Acid Sequence↗
PubMed1993

An acetazolamide-sensitive inward chloride pump in vascular smooth muscle.

In smooth muscle cells, which have a small but significant chloride ion permeability, Cl:HCO3 exchange and (Na+K+Cl) cotransport are known to act as inwardly directed chloride pumps. However, even allowing for overestimation of [Cl]i due to intracellular interference with the Cl-recording electrodes, there remained a residual accumulation of chloride in rat arterial smooth muscle under conditions in which neither of these processes is operative. Manipulation of [Cl]i and Cl permeability using pharmacological agents whilst monitoring both Em and [Cl]i showed that an acetazolamide-sensitive mechanism, perhaps a Cl-dependent ATPase, is the third pathway for Cl accumulation.

Acetazolamide↗
PubMedDate not supplied

Acquired smooth muscle hamartoma.

Smooth muscle hamartoma is an uncommon, usually congenital, cutaneous hyperplasia of the arrectores pilorum muscles. When it is acquired, it may be confused with Becker's nevus. We report a case of this rare tumor in a 19-year-old man. The disease started several years ago as multiple small skin-colored papules that subsequently coalesced to form a large soft plaque on the back of the left shoulder. The diagnosis of acquired smooth muscle hamartoma was confirmed on histopathology. The patient was reassured about the benign nature of the lesion and was not advised any treatment.

Adult↗
PubMed2004

Electrodynamic smooth muscle sphincter: development and biomechanical evaluation of a novel porcine artificial smooth muscle sphincter in a new in vitro stoma simulator.

AIM: Many authors have suggested that the activity of the enteric inhibitory nerves is important in regulating normal gastrointestinal motility and inducing smooth muscle relaxation. Hitherto, no experimental or clinical models exist that transfer these physiological aspects to creating an autologous artificial sphincter for the treatment of major incontinence. Therefore, this study was performed to determine the contractile and relaxant capacity of gastrointestinal muscle types and to investigate the efficiency of a novel smooth muscle sphincter, based on the non-adrenergic, non-cholinergic (NANC) receptive relaxation under electrical field stimulation (EFS). METHODS: For the first step, the isometric tension from isolated circular porcine fundus and colon muscle strips was recorded during pharmacological stimulation (TTX, L-NNA and atropine) and EFS. As a result, a continent electrodynamic smooth muscle sphincter (ESMS) was created by wrapping a fundus muscle flap around an isolated segment of porcine distal colon. The EFS of the free nerve fibers of the flap was realized using a circular platinum wire electrode. Parameters such as threshold of continence, intra/preluminal pressure and fluid passage were analyzed in a newly designed in vitro stoma simulator. RESULTS: Electrical field stimulation produced a maximal and voltage-dependent fundus relaxation to --12.4 mN/mm(2) (frequency of 40 Hz, pulse duration, train duration and voltage of 5 ms, 1 s and 60 mA respectively), which were abolished by N-nitro-L -arginine (L-NNA; 10(-4) M) in a dose-dependent manner, confirming that relaxant responses were mediated by NANC nerves. The results of eight ESMS showed that circular electrical stimulation of the muscle flap caused muscle relaxation with a concomitant and effective reduction in the occlusion pressure. CONCLUSION: The NANC-induced relaxation mechanism of porcine fundus preparations could be transferred to an efficient smooth muscle sphincter with a high threshold of continence and electrically controlled defecation.

Anal Canal↗
PubMed1983

Contraction and [3H]QNB binding in collagenase isolated fundic smooth muscle cells.

Smooth muscle cells from the guinea pig gastric fundus were isolated by successive collagenase digestions. Tritiated quinuclidinyl benzilate [( 3H]QNB) was used to study the binding characteristics of the muscarinic cholinergic receptors on these cells. Each cell bound 8.3 X 10(-19) mol of QNB, and a concentration of QNB of 0.19 nM was required to label one-half of the binding sites. This suggests a concentration of about 500,000 muscarinic cholinergic receptors per smooth muscle cell. The muscarinic cholinergic receptor antagonists atropine and scopolamine inhibited QNB binding with a 50% inhibiting concentration (IC50) in the nanomolar range, whereas the agonists acetylcholine (ACh), oxotremorine, and carbamylcholine had IC50S in the micromolar range. Hill coefficients (nH) for antagonists approached unity, but agonists displayed fractional nH. Exposure of cells to cholinergic muscarinic agonists resulted in dose-dependent decreases in cell length. The concentration of agonist required to induce half-maximal contractions (ED50) was 8.3 X 10(-12) M for ACh and 6.3 X 10(-13) M for oxotremorine. Atropine (10(-9) M) decreased the sensitivity to ACh, increasing the ED50 for ACh-induced contractions to 1.2 X 10(-10) M. These results suggest the existence of muscarinic receptor heterogeneity for cholinergic agonists but not for antagonists.

Acetylcholine↗
PubMed1983

Compartmentation of glycolytic and glycogenolytic metabolism in vascular smooth muscle.

Vascular smooth muscle is characterized by a high rate of aerobic lactate production, which may be altered independently of oxidative phosphorylation. This finding suggested a cytoplasmic compartmentation of metabolism. Exogenous glucose was found to be the sole precursor of aerobic glycolysis under unstimulated conditions. Although tissue depolarization with high K+ resulted in a substantial reduction of endogenous glycogen, exogenous glucose remained the sole precursor of aerobic lactate production. These data showed unequivocally that carbohydrate metabolism is compartmentalized in vascular smooth muscle.

Animals↗