Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Muscle, Smooth”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 433 records · Page 24Linked to original sources
PubMed1991

The role of vascular smooth-muscle cells in atherogenesis: phenotypic modulation of the medial smooth-muscle cells in the aortic bifurcation.

To elucidate the mechanism of migration of vascular smooth-muscle cells (SMCs) from media to intima, we have investigated the phenotypic modulation of the medial SMC at bifurcation of the celiac artery in 5 children and 3 young persons using a transmission electron microscope. We counted the number of separated SMCs from the elastic layers, although the medial SMCs are fundamentally attached to the elastic fibers, and are still contractile in their phenotypes. Both proximal and distal portions revealed that SMCs in the media were more or less present in the separated state and were ultrastructurally consistent with the synthetic state of SMC in the proximal area and the contractile state in distal areas. In order to migrate from media to intima, medial SMC should separate from the elastic layers and transform their phenotypes. In this paper, we examined the relationship between vascular SMCs and elastic layers in the media and ascertain that it was responsible for the contribution to the subsequent phenotypic modulation and their migration of medial SMCs.

Adolescent↗
PubMed1984

Effect of skeletal muscle relaxants on bladder smooth muscle.

The present study was conducted to determine the effects of skeletal muscle relaxants on contractions of bladder smooth muscle. Rat, rabbit and human bladder muscle strips were incubated in a 50 ml. organ bath filled with physiological salt solution, aerated with 95 per cent O2, 5 per cent CO2 and maintained at 37C. Contractions were induced both electrically and with acetylcholine. Contractile strength was measured before and after 30 to 70 minute incubations with diazepam (0.25 to 1.0 microgram./ml.), dantrolene sodium (4 micrograms./ml.) or baclofen (4 micrograms./ml.). Neither baclofen nor dantrolene sodium had any effect (p greater than 0.3) on electrically or acetylcholine-induced contractions in any of the 3 species tested but diazepam potentiated both electrically induced (115 per cent of predrug contractile strength, p less than 0.05) and acetylcholine-induced (122 per cent of predrug contractile strength, p less than 0.01) contractions of rat, but not rabbit or human, bladder muscle. In rabbits diazepam significantly reduced maximal bladder pressures in vivo (p less than 0.05) but had no effect on bladder capacity. Dantrolene sodium had no effect on rabbit bladder pressure or capacity in vivo. While diazepam is thought to exert its effects on skeletal muscle through CNS inhibition, these results suggest that diazepam may affect rat but not rabbit or human bladder smooth muscle directly.

Acetylcholine↗
PubMed2006

Cultured smooth muscle cells of the human vesical sphincter are more sensitive to histamine than are detrusor smooth muscle cells.

OBJECTIVES: To compare histamine receptor expression in cultured smooth muscle cells from the human detrusor and internal sphincter using receptor-specific agonists. METHODS: Smooth muscle cells from the bladder dome and internal sphincter were cultured from 5 male patients undergoing cystectomy for bladder cancer therapy. Calcium transients in cells stimulated with carbachol, histamine, histamine receptor 1 (H1R)-specific heptanecarboxamide (HTMT), dimaprit (H2R), and R-(alpha)-methylhistamine (H3R) were measured by calcium imaging. Histamine receptor proteins were detected by Western blot analysis and immunocytochemistry. RESULTS: H1R, H2R, and H3R expression was found in tissue and cultured cells. Carbachol stimulated equal numbers of detrusor and sphincter cells (60% and 51%, respectively). Histamine stimulated significantly more cells than carbachol in detrusor (100%) and sphincter (99.34%) cells. Calcium responses to carbachol in detrusor and sphincter cells were comparable and did not differ from those to histamine in detrusor cells. However, histamine and specific agonists stimulated more sphincter cells than did carbachol (P <0.001), and the calcium increase was greater in sphincter cells than in detrusor cells. Single cell analysis revealed comparable H2R responses in detrusor and sphincter cells, but H1R and H3R-mediated calcium reactions were significantly greater in sphincter cells. CONCLUSIONS: Histamine very effectively induces calcium release in smooth muscle cells. In sphincter cells, histamine is even more effective than carbachol regarding the number of reacting cells and the intracellular calcium increase. Some of the variability in the outcome of antihistaminic interstitial cystitis therapies might be caused by the ineffectiveness of the chosen antihistaminic or unintentional weakening of sphincteric function.

Calcium↗
PubMed2003

Expression of the ether-a-go-go (ERG) potassium channel in smooth muscle of the equine gastrointestinal tract and influence on activity of jejunal smooth muscle.

OBJECTIVE: To determine whether ether-a-go-go (ERG) potassium channels are expressed in equine gastrointestinal smooth muscle, whether ERG channel antagonists affect jejunal muscle contraction in vitro, and whether plasma cisapride concentrations in horses administered treatment for postoperative ileus (POI) are consistent with ERG channels as drug targets. SAMPLE POPULATION: Samples of intestinal smooth muscle obtained from 8 horses free of gastrointestinal tract disease and plasma samples obtained from 3 horses administered cisapride for treatment of POI. PROCEDURE: Membranes were prepared from the seromuscular layer of the duodenum, jejunum, ileum, cecum, large colon, and small colon. Immunoblotting was used to identify the ERG channel protein. Isolated jejunal muscle strips were used for isometric stress response to ERG channel blockers that included E-4031, MK-499, clofilium, and cisapride. Plasma concentrations of cisapride were determined in 3 horses administered cisapride for treatment of POI after small intestinal surgery. RESULTS: Immunoblotting identified ERG protein in all analyzed segments of the intestinal tract in all horses. The selective ERG antagonist E-4031 caused a concentration-dependent increase in jejunal contraction. Clofilium, MK-499, and cisapride also increased jejunal contraction at concentrations consistent with ERG channel block; effects of E-4031 and cisapride were not additive. Peak plasma cisapride concentrations in treated horses were consistent with ERG block as a mechanism of drug action. CONCLUSIONS AND CLINICAL RELEVANCE: The ERG potassium channels modulate motility of intestinal muscles in horses and may be a target for drugs. This finding may influence development of new prokinetic agents and impact treatment of horses with POI.

Animals↗
PubMedDate not supplied

Diffusable growth factors induce bladder smooth muscle differentiation.

Bladder smooth muscle differentiation is dependent on the presence of bladder epithelium. Previously, we have shown that direct contact between the epithelium and bladder mesenchyme (BLM) is necessary for this interaction. In this study, we tested the hypothesis that bladder smooth muscle can be induced via diffusable growth factors. Fourteen-day embryonic rat bladders were separated into bladder mesenchyme (prior to smooth muscle differentiation) and epithelium by enzymatic digestion and microdissection. Six in vitro experiments were performed with either direct cellular contact or no contact (1) 14-d embryonic bladder mesenchyme (BLM) alone (control), (Contact) (2) 14-d embryonic bladders intact (control), (3) 14-d embryonic bladder mesenchyme combined with BPH-1 cells (an epithelial prostate cell line) in direct contact, (4) 14-d embryonic bladder mesenchyme with recombined bladder epithelium (BLE) in direct contact, (No Contact) (5) 14-d embryonic bladder mesenchyme with BPH-1 prostatic epithelial cells cocultured in type 1 collagen gel on the bottom of the well, and (6) 14-d embryonic bladder mesenchyme with BPH-1 epithelium cultured in a monolayer on a transwell filter. In each case the bladder tissue was cultured on Millicell-CM 0.4-microm membranes for 7 d in plastic wells using serum free medium. Growth was assessed by observing the size of the bladder organoids in histologic cross section as well as the vertical height obtained in vitro. Immunohistochemical analysis of the tissue explants was performed to assess cellular differentiation with markers for smooth muscle alpha-actin and pancytokeratin to detect epithelial cells. Control (1) bladder mesenchyme grown alone did not exhibit growth or smooth muscle and epithelial differentiation. Contact experiments (2) intact embryonic bladder, (3) embryonic bladder mesenchyme recombined with BPH-1 cells, and (4) embryonic bladder mesenchyme recombined with urothelium each exhibited excellent growth and bladder smooth muscle and epithelial differentiation. Both noncontact experiments (5) and (6) exhibited growth as well as bladder smooth muscle and epithelial differentiation but to a subjectively lesser degree than the contact experiments. Direct contact of the epithelium with bladder mesenchyme provides the optimal environment for growth and smooth muscle differentiation. Smooth muscle growth and differentiation can also occur without direct cell to cell contact and is not specific to urothelium. This data supports the hypothesis that epithelium produces diffusable growth factors that induce bladder smooth muscle.

Animals↗
PubMed1986

Aggregation of smooth muscle membranes and its use in the preparation of plasma membrane enriched fraction from gastric fundus smooth muscle.

Microsomal membranes isolated from rat gastric fundus smooth muscle by differential centrifugation aggregate substantially in the presence of the divalent metal ion Mg2+ or Ca2+. The magnitude of cation-induced membrane aggregation is higher for Ca2+ than for Mg2+, but the ion concentration required for half-maximum membrane aggregation (K0.5 value) is similar for Mg2+ and Ca2+. Cation-induced membrane aggregation is suppressed by high ionic strength and low pH of the medium. Cation-induced membrane aggregation of mitochondrial membrane and plasma membrane enriched fractions differ in the rate of aggregate formation, metal ion concentration dependence, and pH dependence. Such different properties of membrane aggregation were used to prepare a plasma membrane enriched fraction by conventional differential centrifugation. Subfractionation of the heterogeneous microsomal membranes by free-flow electrophoresis indicated that smooth muscle plasma membranes showed a higher electrophoretic mobility than the intracellular membranes. These results suggest that ionic interactions on the cell membrane surfaces differ from those on the intracellular membrane surfaces and that induction of membrane aggregation by Ca2+ or Mg2+ is a useful procedure for an effective and rapid preparation of plasma membrane enriched fraction from smooth muscle.

Animals↗
PubMed1993

Expression of elastin, smooth muscle alpha-actin, and c-jun as a function of the embryonic lineage of vascular smooth muscle cells.

In the avian embryo, vascular smooth muscle cells (VSMC) in the aortic arch (elastic) arteries originate in the neural crest, whereas other VSMC develop from local mesoderm. These two lineages have been shown previously to be significantly different in the timing and expression of the smooth muscle phenotype and in their respective abilities to produce an orderly elastic matrix. Two differing kinds of VSMC also have been shown in mammals. In the experimental absence of neural crest (NC) in the avian embryo, the matrix is spatially disordered. The molecular basis of the difference between the normal NC-VSMC and the surrogate mesodermal (MDM)-VSMC has not previously been investigated. In this study the expression of vascular smooth muscle alpha-actin, tropoelastin, c-fos and c-jun were examined via immunoblotting, immunohistochemistry, Northern blot, and/or transcription run-on assays. Control avian VSMC of NC origin were compared with experimental MDM-derived VSMC that populate the cardiac outflow after surgical ablation of the NC. The results show that, when they are grown under identical conditions in vitro or freshly removed from an embryonic vessel, surrogate MDM-VSMC express about 10 times more alpha-actin and tropoelastin than the normal NC-VSMC; and MDM-VSMC express up to 15 times more c-jun, whereas c-fos was not different. These results show profound heterogeneity in the regulation of VSMC-specific genes that is based in the embryonic lineage of the cells.

Actins↗
PubMed2006

Airway smooth muscle and mast cell-derived CC chemokine ligand 19 mediate airway smooth muscle migration in asthma.

RATIONALE: Airway smooth muscle (ASM) hyperplasia is a feature of asthma, and increases with disease severity. We hypothesized that this results from migration of ASM or progenitors in response to chemokines derived from ASM or mast cells within the ASM bundle. OBJECTIVES: To examine expression of the chemokine receptor, CC chemokine receptor (CCR) 7, in vivo by ASM in patients with asthma and healthy control subjects, and by primary cultures of ASM and fibroblasts; to define expression of its ligands, CC chemokine ligand (CCL) 19 and CCL21, in bronchial biopsies, and primary cultures of ASM and mast cells; and to investigate CCR7's role in ASM migration and repair. METHODS: ASM was isolated from bronchoscopy and resection tissue. Receptor and chemokine expression was examined by immunohistochemistry, immunofluorescence, flow cytometry, ELISA, and reverse transcriptase-polymerase chain reaction. CCR7 function was examined by intracellular calcium measurements, chemotaxis, wound healing assays, and measurement of cell proliferation. MEASUREMENTS AND MAIN RESULTS: ASM, myofibroblasts, and fibroblasts expressed CCR7. CCL19, but not CCL21, was highly expressed in bronchial biopsies by mast cells and vessels in asthma of all severities, ASM in severe disease, and ex vivo ASM and mast cells. ASM CCR7 activation by CCL19-mediated intracellular calcium elevation and concentration-dependent migration, but not proliferation. Importantly, mast cell and ASM-derived CCL19 mediated ASM migration and repair. CONCLUSIONS: The CCL19/CCR7 axis may play an important role in the development of ASM hyperplasia in asthma.

Asthma↗
PubMed1975

Effect of castration on the smooth muscle cells of the internal sex organs of the rat: influence of the smooth muscle on the sympathetic neurons innervating the vas deferens, seminal vesicle and coagulating gland.

Wet weights of vas deferens, seminal vesicle and coagulating gland were reduced by almost 80 to 90% 10 weeks after castration. Endogenous norepinephrine content and dopamine-beta-hydroxylas activity of these tissues were also reduced to the same degree. One week after castration there was approximately a 50% loss in the weight of all three organs. However, this was accompanied by an equal reduction in norepinephrine content and dopamine-beta-hydroxylase activity only in the vas deferens. Two weeks later the degree of reductions in wet weight, norepinephrine content and dopamine-beta-hydroxylase activity was almost identical for all three organs. Treatment of 40-day castrate rats with testosterone (10 mg/kg s.c.) not only restored the wet weights of the internal sex organs to normal but their norepinephrine content and dopamine-beta-hydroxylase activity as well. Castration of immature rats (10-14 days old) resulted in retardation of growth of the vas deferens and seminal vesicle by 90-95%, and similar reductions in norepinephrin content and dopamine-beta-hydroxylase activity, when compared to the tissues of control littermates on the 90th postoperative day. Histological examination of normal and castrate rats indicated that, along with a reduction in epithelial cells, the smooth muscle cells of the vas deferens, seminal vesicle and coagulating gland was markedly reduce in size as well. Administration of testosterone completely reversed these changes. Furthermore, deoxyribonucleic acid content of the seminal vesicle and coagulating gland was reduced by 50% after castration and then restored to control level after testosterone treatment. Taken together, it seems that atrophy of the internal sex organs following castration is a combined effect of reduction in size and number of smooth muscle cells. Therefore, it is concluded that any alteration in the size of smooth muscle cells or loss of such cells of the internal sex organs indirectly influences their sympathetic nerves in such a manner that norepinephrine concentrations, and thereby the density of innervation, are maintained at normal levels.

Animals↗
PubMed2004

Over expression of smooth muscle specific caldesmon by transfection and intermittent agonist induced contraction alters cellular morphology and restores differentiated smooth muscle phenotype.

PURPOSE: The thin filament associated protein h-caldesmon (h-CaD) modulates actin myosin interaction and contraction. Bladder outlet obstruction and detrusor hypertrophy are associated with the over expression of the nonmuscle CaD isoform l-CaD. It implies a poorly differentiated state of bladder myocytes and cytoskeletal remodeling in detrusor hypertrophy. We determined if h-CaD expression can be increased in a unique bladder smooth muscle (BSM) cell line derived from obstructed rabbit bladder smooth muscle that over expresses l-CaD. We examined whether the genetic restoration of h-caldesmon is possible in bladder smooth muscle cells by transfection or by agonist mediated contraction and whether this manipulation would alter cellular morphology. MATERIALS AND METHODS: BSM cells were transfected with chicken h-CaD cDNA inserted into a mammalian vector. In another experiment BSM cells underwent intermittent bethanechol induced stimulation. h-CaD mRNA and protein were quantified with reverse transcriptase-polymerase chain reaction and Western blot analyses. Cell morphology was assessed using phase, video and confocal microscopy after double immunostaining with antibodies against alpha-actin and caldesmon. RESULTS: Reverse transcriptase-polymerase chain reaction using primers specific for the transfected vector and h-CaD cDNA confirmed stable transfection of cells and increased content of h-CaD mRNA. Following bethanechol induced intermittent contraction Western blotting revealed 80% relative over expression of h-CaD in treated transfected cell lines (p <0.05) and 74% (not significant) in treated nontransfected controls. Confocal immunofluorescence microscopy revealed CaD in the cytoplasmic filaments co-localized to alpha-actin in the main cell body and perinuclear region in transfected cells, in contrast to the diffuse, irregular distribution of these filaments in control cells. CONCLUSIONS: A unique bladder myocyte cell line was successfully and stably transfected with h-CaD cDNA. We show that agonist induced intermittent contraction preferentially increases h-CaD expression, the predominant CaD in nonobstructed bladder smooth muscle, and the restoration of h-CaD alters cell morphology and the organization of cytoplasmic filaments in cells derived from obstructed rabbit detrusor musculature.

Bethanechol↗
PubMed2000

Serum response factor-dependent regulation of the smooth muscle calponin gene.

Smooth muscle calponin is a multifunctional, thin filament-associated protein whose expression is restricted to smooth muscle cell lineages in developing and postnatal tissues. Although the physiology of smooth muscle calponin has been studied extensively, the cis-elements governing its restricted pattern of expression have yet to be identified. Here we report on smooth muscle-specific enhancer activity within the first intron of smooth muscle calponin. Sequence analysis revealed a proximal consensus intronic CArG box and two distal intronic CArG-like elements, each of which bound recombinant serum response factor (SRF) as well as immunoreactive SRF from smooth muscle nuclear extracts. Site-directed mutagenesis studies suggested that the consensus CArG box mediates much of the intronic enhancer activity; mutating all three CArG elements abolished the ability of SRF to confer enhancer activity on the smooth muscle calponin promoter. Cotransfecting a dominant-negative SRF construct attenuated smooth muscle-specific enhancer activity, and transducing smooth muscle cells with adenovirus harboring the dominant-negative SRF construct selectively reduced steady-state expression of endogenous smooth muscle calponin. These results demonstrate an important role for intronic CArG boxes and the SRF protein in the transcriptional control of smooth muscle calponin in vitro.

Animals↗
PubMed1997

Smooth muscle heterogeneity: does the striated muscle model apply?

Smooth muscle cells are the major component of most smooth muscle tissue. Although the function of these tissues is known to differ, it has been generally assumed that the smooth muscle cells that make up these tissues are all the same. In striated muscle, individual fibers composed of unique contractile and regulatory proteins have unique mechanical properties. Smooth muscles also contain unique proteins. The hexamer myosin has multiple isoforms of its heavy and light chain subunits. Some of these differences result from alternate splicing of a single gene, while others result from multiple genes. At the tissue level, the presence of these isoforms is developmentally regulated and varies between tissues and species. There are numerous contradictory reports in the literature regarding possible unique regulation and function for the multiple myosin heavy and light chain isoforms. By extending molecular and mechanical methods beyond their normally used ranges, we have begun a series of experiments at the single smooth muscle cell level. Preliminary results show extreme heterogeneity of myosin isoforms between smooth muscle cells. In addition, preliminary results suggest that the ratio of the SM1 and SM2 MHC tail isoforms do not correlate with unloaded shortening velocity. However, there is a good correlation between the amount of SM2 MHC isoform present in the cell and the minimum length to which the cell can shorten. Thus, cells with a greater SM2 content appear to shorten more than cells with a lesser SM2 content. As with striated muscle, single-cell experiments may be required to determine the unique function of protein isoforms in smooth muscle tissues.

Animals↗
PubMed1991

Sodium cotransport in vascular smooth muscle cells.

Vascular smooth muscle cells possess a number of Na cotransport systems. Three of these cotransport systems, Na/Ca exchange, Na/H exchange and Na-K-Cl cotransport, have been the subject of an increasing number of investigations to determine the respective roles of these transporters in vascular smooth muscle cell function. Evidence has been obtained that the Na/Ca exchange system participates in regulation of intracellular Ca in vascular smooth muscle cells. The Na/H exchange system appears to function in concert with a Cl/HCO3 exchange system to regulate intracellular pH. The Na-K-Cl cotransport system is a major contributor to K flux across the plasma membrane of vascular smooth muscle cells and is regulated by a number of vasoactive agents, suggesting that this Na cotransport system is also an important component of vascular smooth muscle cell function. Cultured vascular smooth muscle cells derived from spontaneously hypertensive rats have been found to exhibit reduced Na-K-Cl cotransport activity compared to smooth muscle cells from normotensive controls. Thus, alteration of vascular smooth muscle Na-K-Cl cotransport activity may be related to changes in vascular tone. However, the precise function of Na-K-Cl cotransport in vascular smooth muscle cells remains to be clarified. Recent studies of Na-K-Cl cotransport in vascular endothelial cells provide evidence that the co-transporter is important for regulation of endothelial cell volume and suggest that this Na cotransport system may be vitally important for normal function of the vasculature.

Animals↗
PubMed1989

Differential effect of platelet-derived growth factor- versus serum-induced growth on smooth muscle alpha-actin and nonmuscle beta-actin mRNA expression in cultured rat aortic smooth muscle cells.

Previous studies have demonstrated that rat aortic smooth muscle cells (SMC) show marked changes in smooth muscle (SM) alpha-actin content and fractional synthesis as a function of cell density and growth (Owens, G. K., Loeb, A., Gordon, D., and Thompson, M. M. (1986) J. Cell Biol. 102, 343-352; Blank, R., Thompson, M. M., and Owens, G. K. (1988) J. Cell Biol. 107, 299-306). Results of this study show that, although there is a 6-fold increase in SM alpha-actin content in postconfluent density arrested cultures as compared to proliferating subconfluent cultures, SM alpha-actin mRNA levels are not different between these cells. This suggests that the SM alpha-actin gene is constitutively active under both of these conditions and that accumulation of SM alpha-actin in postconfluent cells is due to translational and/or post-translational controls. The relationship between growth and cytodifferentiation was further explored by examining the effects of platelet-derived growth factor (PDGF)- or serum-induced growth on actin expression in postconfluent, quiescent cultures maintained in a defined serum-free media. Although both factors have been shown to stimulate proliferation and decrease fractional SM alpha-actin synthesis (Blank et al., 1988), their effects on actin mRNA levels were quite different. PDGF was found to induce a dramatic drop in SM alpha-actin steady state mRNA level but had no effect on nonmuscle beta-actin mRNA level. In contrast, serum stimulation was shown to increase nonmuscle beta-actin mRNA level, whereas SM alpha-actin mRNA level remained constant. Taken together these results indicate that PDGF is a specific and potent repressor of SM alpha-actin expression in vascular SMC and implicate a possible developmental role for PDGF in control of SMC differentiation. In addition, the observation that the level of SM alpha-actin mRNA is unaltered in serum-stimulated cells indicates that an absolute decrease in SM alpha-actin mRNA is not obligatory for cell cycle entrance.

Actins↗