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PubMed1979

Glycoprotein, elastin, and collagen secretion by rat smooth muscle cells.

Smooth muscle cells from rat heart secreted extracellular matrix components at high rates for many generations in culture. The matrix proteins remained anchored to the culture dish and were characterized after removal of cellular material with sodium dodecyl sulfate. Sequential enzyme digestion demonstrated the presence of at least three components, including glycoprotein(s), elastin, and collagen. Prolonged extraction of the matrix with detergent under reducing conditions solubilized a fucosylated glycoprotein having an apparent molecular weight of 250,000 and two other proteins with molecular weights of 72,000 and 45,000, respectively. Sublines derived from discrete colonies of smooth muscle cells synthesized all of the matrix components, and the proportion of collagen secreted by some sublines increased with time in culture. The biosynthesis of a mixed extracellular matrix and the relationships among the component proteins were therefore studied in one system producing milligram quantities of material.

Animals↗
PubMed1993

Ionic basis of the action potential of guinea pig gallbladder smooth muscle cells.

Smooth muscle cells in the intact guinea pig gallbladder had a resting membrane potential of about -45 mV and had spontaneous action potentials that consisted of a rapid depolarization, a transient repolarization, a plateau phase, and a complete repolarization. These action potentials lasted approximately 570 ms and occurred at a frequency of approximately 0.4 Hz. Action potentials were abolished by the dihydropyridine (DHP)-sensitive Ca2+ channel blocker nifedipine (1.0 microM) and were enhanced by the DHP-sensitive Ca2+ channel agonist BAY K 8644 (0.5 microM). The K+ channel blockers tetraethylammonium chloride (5.0 mM) and 4-aminopyridine (4-AP; 2.0 mM) prolonged the action potential, whereas charybdotoxin (100 nM), a blocker of calcium-activated potassium channels, had no effect. Whole cell currents were characterized in enzymatically isolated smooth muscle cells from the same preparation. 4-AP, a blocker of voltage-dependent K+ channels, suppressed 70% of the outward current at 0 mV. Charybdotoxin (100 nM) reduced an additional 15% of the current at 0 mV. Single calcium-activated potassium channels were identified. The potential for half-activation of these channels, at a cytosolic Ca2+ concentration of 100 nM, was 66.8 mV. A fivefold increase in cytosolic Ca2+ resulted in a shift of the activation curve by -53 mV. External tetraethylammonium chloride (200 microM) reduced the mean single channel current by 48% at 0 mV. The whole cell outward current was abolished by replacement of intracellular K+ for Cs+. Ca2+ currents were inhibited by nifedipine and were increased by BAY K 8644. We conclude that DHP-sensitive voltage-dependent Ca2+ channels are responsible for the depolarization of the action potentials and that the repolarization is due to primarily 4-AP-sensitive K+ current.

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

Calcium utilization by dispersed canine gastric smooth muscle cells.

Smooth muscle cells were isolated by collagenase digestion from the circular layer of the canine gastric corpus, and cell length was measured by image-splitting micrometry. Cells contracted following incubation with KCl, carbachol, and pentagastrin. While contraction induced by 40 mM KCl was inhibited by adding nitrendipine (10 nM) or by removing extracellular calcium and adding EGTA (2 mM), the contraction induced by carbachol (10 pM) was not affected by these measures. Nitrendipine partially inhibited contraction induced by pentagastrin, and pentagastrin also contracted cells that had been depolarized by prior exposure to KCl and nitrendipine. Removing extracellular calcium and adding EGTA partially inhibited contraction induced by maximally (10 pM) or submaximally effective (0.3 pM) concentrations of pentagastrin but did not affect that induced by 300 pM pentagastrin. These results indicate that isolated smooth muscle cells utilize calcium for contraction by three distinct mechanisms. The extent to which each mechanism contributes to contraction depends on the nature of the stimulus and, in the case of pentagastrin, the concentration of the stimulating ligand.

Animals↗
PubMed2004

Smooth muscle archvillin: a novel regulator of signaling and contractility in vascular smooth muscle.

The mechanisms by which protein kinase C (PKC) and extracellular-signal-regulated kinases (ERK1/2) govern smooth-muscle contractility remain unclear. Calponin (CaP), an actin-binding protein and PKC substrate, mediates signaling through ERK1/2. We report here that CaP sequences containing the CaP homology (CH) domain bind to the C-terminal 251 amino acids of smooth-muscle archvillin (SmAV), a new splice variant of supervillin, which is a known actin- and myosin-II-binding protein. The CaP-SmAV interaction is demonstrated by reciprocal yeast two-hybrid and blot-overlay assays and by colocalization in COS-7 cells. In differentiated smooth muscle, endogenous SmAV and CaP co-fractionate and co-translocate to the cell cortex after stimulation by agonist. Antisense knockdown of SmAV in tissue inhibits both the activation of ERK1/2 and contractions stimulated by either agonist or PKC activation. This ERK1/2 signaling and contractile defect is similar to that observed in CaP knockdown experiments. In A7r5 smooth-muscle cells, PKC activation by phorbol esters induces the reorganization of endogenous, membrane-localized SmAV and microfilament-associated CaP into podosome-like structures that also contain F-actin, nonmuscle myosin IIB and ERK1/2. These results indicate that SmAV contributes to the regulation of contractility through a CaP-mediated signaling pathway, involving PKC activation and phosphorylation of ERK1/2.

Alternative Splicing↗
PubMed1992

Voltage-dependent calcium current and the effects of adrenergic modulation in rat aortic smooth muscle cells.

Smooth muscle cells from rat aorta were cultured in defined, serum-free medium and studied using whole-cell patch-clamp techniques. Under conditions designed to isolate currents through Ca channels, step depolarizations produced inward currents which were fast in onset and inactivated rapidly, with little sustained inward current being observed. Both Ni and Cd blocked these currents, with Ni being effective at 50 microM. Removal of external Na or addition of 1 microM tetrodotoxin had no effect. Peak inward currents were attained at about -15 mV, with half-maximal activation at -41 mV using -80 mV holding potentials. The transient inward currents were reduced by depolarized holding potentials, with half-maximal steady-state inactivation at -48 mV. In three of the 98 cells studied, small maintained inward currents were observed with a -40 mV holding potential. The Ca channel antagonist nicardipine (5 microM) blocked the transient inward current while neither of the dihydropyridine Ca channel agonists S(+)202 791 and (-)BAY K 8644 produced a significant augmentation of sustained inward current. At 10 microM, both noradrenaline and adrenaline but not phenylephrine decreased the peak inward current. This inhibition was unaffected by a variety of adrenoceptor antagonists and was also observed when internal solutions having high Ca buffering capacity were used, but was absent when GDP-beta-S instead of GTP was included in the pipette solution. The main conclusions from this study are that under our cell culture conditions, rat aortic smooth muscle cells possess predominantly a transient, low-threshold-activated inward Ca current and that this Ca current is inhibited by certain adrenoceptor agonists but with a quite atypical adrenoceptor antagonist pharmacology.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2005

Fgf10 expression identifies parabronchial smooth muscle cell progenitors and is required for their entry into the smooth muscle cell lineage.

Lineage formation in the lung mesenchyme is poorly understood. Using a transgenic mouse line expressing LacZ under the control of Fgf10 regulatory sequences, we show that the pool of Fgf10-positive cells in the distal lung mesenchyme contains progenitors of the parabronchial smooth muscle cells. Fgf10 gene expression is slightly repressed in this transgenic line. This allowed us to create a hypomorphic Fgf10 phenotype by expressing the LacZ transgene in a heterozygous Fgf10 background. Hypomorphic Fgf10 mutant lungs display a decrease in beta-galactosidase-positive cells around the bronchial epithelium associated with an accumulation of beta-galactosidase-expressing cells in the distal mesenchyme. This correlates with a marked reduction of alpha smooth muscle actin expression, thereby demonstrating that FGF10 is mostly required for the entry of mesenchymal cells into the parabronchial smooth muscle cell lineage. The failure of exogenous FGF10 to phosphorylate its known downstream targets ERK and AKT in lung mesenchymal cultures strongly suggests that FGF10 acts indirectly on the progenitor population via an epithelial intermediate. We provide support for a role of epithelial BMP4 in mediating the formation of parabronchial smooth muscle cells.

Actins↗
PubMed1996

Mechanical strain increases smooth muscle and decreases nonmuscle myosin expression in rat vascular smooth muscle cells.

The effect of cyclic (1-Hz) mechanical strain on expression of myosin heavy chain isoforms was examined in neonatal rat vascular smooth muscle cells cultured on silicone elastomer plates. Myosin heavy chain isoforms were identified by immunoblot using antibodies recognizing (1) smooth muscle myosin heavy chain isoforms SM-1 and SM-2, (2) SM-1 exclusively, and (3) nonmuscle myosin heavy chains A and B. In response to 36 to 72 hours of strain, SM-1 and SM-2 increased by fourfold to sixfold, whereas nonmuscle myosin A decreased to 30% of control. Nonmuscle myosin B was unaffected by strain. SM-1 mRNA increased by twofold to threefold after 12 hours of strain but decreased toward control levels thereafter. SM-2 mRNA was only barely detectable. Nonmuscle myosin A mRNA decreased to 50% of control after 3 hours of strain and then returned to the control level. Since these cells secrete platelet-derived growth factor (PDGF) in response to strain, we assessed the effects of PDGF on myosin isoform expression. Exogenous PDGF (10 ng/mL) decreased SM-1 expression by 35% and increased nonmuscle myosin expression twofold, opposite the effect of strain. In cells exposed to strain with neutralizing antibodies to PDGF-AB, the strain-induced increase in SM-1 was enhanced 10-fold, and nonmuscle myosin A was reduced to 40% of control. Finally, the effect of extracellular matrix on transduction of the strain signal was studied. Forty-eight hours of cyclic strain increased SM-1 by twofold in cells cultured on collagen type 1 and threefold in cells cultured on laminin. In fibronectin-cultured cells, strain elicited no increase in SM-1. Thus, mechanical strain, sensed through specific interactions with the matrix, can alter myosin isoform expression toward that found in a more differentiated state.

Animals↗
PubMed2000

Differential display identification of 40 genes with altered expression in activated human smooth muscle cells. Local expression in atherosclerotic lesions of smags, smooth muscle activation-specific genes.

Detailed knowledge on the molecular and cellular mechanisms that control (re)-differentiation of vascular smooth muscle cells (SMCs) is critical to understanding the pathological processes underlying atherogenesis. We identified by differential display/reverse transcriptase-polymerase chain reaction 40 genes with altered expression in cultured SMCs upon stimulation with the conditioned medium of activated macrophages. This set of genes comprises 10 known genes and 30 novel genes, which we call "smags" (for smooth muscle activation-specific genes). To determine the in vivo significance of these (novel) genes in atherogenesis, we performed in situ hybridization experiments on vascular tissue. Specifically, FLICE (Fas-associated death domain-like interleukin-1beta-converting enzyme)-like inhibitory protein (FLIP) is expressed in neointimal SMCs as well as in lesion macrophages and endothelial cells, whereas the expression of the novel genes smag-63, smag-64, and smag-84 is restricted to neointimal SMCs. Characterization of full-length smag-64 cDNA revealed that it encodes a novel protein of 66 amino acids. smag-82 cDNA comprises the complete, unknown, 3'-untranslated region of fibroblast growth factor-5. Collectively, our results illustrate the complex changes of SMC gene expression that occur in response to stimulation with cytokines and growth factors secreted by activated macrophages. Moreover, we identified interesting candidate genes that may play a role in the differentiation of SMCs during atherogenesis.

Adult↗
PubMed1988

Influence of haemoglobin and erythrocytes on the effects of EDRF, a smooth muscle inhibitory factor, and nitric oxide on vascular and non-vascular smooth muscle.

1. The relaxant action of endothelium-derived relaxing factor (EDRF), the smooth muscle inhibitory factor (IF) isolated from the bovine retractor penis (BRP), nitric oxide (NO) and sodium nitroprusside (NaNP) on four vascular and non-vascular smooth muscle preparations has been examined. Their sensitivity to EDRF, the IF and NO was the same, suggesting all might be NO. Sodium nitroprusside produced complete relaxation of the rat anococcygeus at low doses, suggesting an action additional to the intracellular release of NO. 2. Haemoglobin added to solutions of EDRF, activated IF or NO completely removed their relaxant properties, consistent with all three acting by virtue of NO. 3. Suspensions of red blood cells with a haemoglobin concentration equivalent to to that used in the previous experiments were as effective as haemoglobin in abolishing the relaxant effect of EDRF or NO but were ineffective against the activated IF. 4. The similarity in sensitivity of a series of smooth muscles and the binding by haemoglobin are consistent with NO being the active principle of both EDRF and the acid activated IF. The abolition of the effect of EDRF by red blood cells (RBCs) is further confirmation for this hypothesis, but the ineffectiveness of RBCs against acid-activated IF suggests that either the latter is not NO or that it is bound in a way which makes it unable to diffuse through cell membranes.

Animals↗
PubMed1993

Interactions between cultured bovine arterial endothelial and smooth muscle cells: studies on uptake and degradation of low density lipoproteins by smooth muscle cells.

This study was designed to investigate the effects of substances released from non-injured and injured bovine arterial endothelial cells on 125I-low density lipoprotein uptake and degradation by smooth muscle cells in culture. It was demonstrated that endothelial cell-released non-dialysable (molecular weight cut off 12-14000) substances significantly stimulated 125I-low density lipoprotein uptake and degradation by smooth muscle cells. Endothelial cell-released dialysable substances and endothelin-1 did not cause this stimulation. The increase in 125I-low density lipoprotein uptake and degradation by smooth muscle cells could be dissociated from cell proliferation. However, in endothelial cell-smooth muscle cell co-culture 125I-low density lipoprotein uptake and degradation by smooth muscle cells were not stimulated. Injury to endothelial cells by lipid-soluble smoke particles or ultraviolet light, which reduced total cellular protein by 15-25%, enhanced the endothelial cell release of the substances stimulating 125I-low density lipoprotein uptake. The results are discussed in relation to atherogenesis.

Animals↗
PubMed1993

Effects of thrombin receptor activating peptide on phosphoinositide hydrolysis and protein kinase C activation in cultured rat aortic smooth muscle cells: evidence for "tethered-ligand" activation of smooth muscle cell thrombin receptors.

Phosphoinositide hydrolysis and protein kinase C (PKC) activation were examined in response to treatment of rat aortic smooth muscle cells with alpha-thrombin and a seven amino acid thrombin receptor activating peptide (TRAP-7; SFLLRNP). alpha-Thrombin and TRAP-7 stimulated total inositol phosphate (IP) accumulation and phosphorylation of a specific endogenous substrate for activated PKC. Acetylated TRAP-7 and "reverse" TRAP (FSLLRNPNDKYEPF) were ineffective in stimulating signal transduction. The active site inhibitor, MD805 (argatroban), and the anion-binding exosite inhibitor, BMS 180,742, reduced the IP response to alpha-thrombin in a concentration-dependent manner. In contrast, the TRAP-7-induced IP response was not affected by either inhibitor. These data are consistent with the tethered-ligand hypothesis for thrombin receptor activation in rat aortic smooth muscle cells.

Animals↗
PubMedDate not supplied

[Membrane mechanisms of regulating Ca ion concentration in smooth muscle cells. II. System of passive Ca2+ transport in smooth muscles].

The aim of this review is to summarize some current aspects on the membrane mechanisms of energy-independent Ca2+ transport in the smooth muscles. The emphasis is placed on the characteristics of voltage-gated and receptor-operated calcium channels of plasma membrane and two major Ca2+ release channels of sarco(endo)plasmic reticulum: one is activated by IP3 and sensitive to heparin and the other by Ca2+ and sensitive to ryanodine. A brief discussion of the electro- and pharmacomechanical coupling mechanisms in the smooth muscle is given.

Calcium↗
PubMed1995

Interleukin-1 beta induces expression of adhesion molecules in human vascular smooth muscle cells and enhances adhesion of leukocytes to smooth muscle cells.

Increased expression of cell adhesion molecules is an important pathological event during the development of atherosclerosis. The smooth muscle cell (SMC) is one of the cell types present in the atherosclerotic lesion. To evaluate the regulation of adhesion molecules in human vascular SMCs and its possible role, we studied the expression of adhesion molecules in SMCs stimulated with interleukin 1-beta (IL-1 beta), a pleiotropic cytokine that is involved in the pathological development of vascular diseases including atherosclerosis and restenosis. Our data demonstrated that IL-1 beta markedly induced the adhesiveness of human vascular SMCs for monocytes and neutrophils in a concentration (10 pM - 10 nM)- and time (0.5-24 h)-dependent manner. The maximal induced adhesion by IL-1 beta (1 nM) was reached at 4 h, with 4.6-fold and 3.3-fold for monocytes and neutrophils, respectively. This induction was dose-dependently inhibited by the IL-1 receptor antagonist (IL-1 ra). The IL-1 beta-induced expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and E-selectin 1 (ELAM-1) on SMCs was examined by reverse transcription/polymerase chain reaction (RT/PCR). Unstimulated, serum-deprived SMCs expressed a low or undetectable level of mRNA for these adhesion molecules. The expression of ICAM-1 and VCAM-1 but not ELAM-1 mRNA was significantly induced with IL-1 beta in a concentration (1 fM - 1 nM)- and time (0.5 - 24 h)-dependent manner. The maximal increase in ICAM-1 and VCAM-1 mRNAs was reached at 4 h after IL-1 beta stimulation. The IL-1 beta-induced adhesion of SMCs for monocytes was partially inhibited by monoclonal anti-human ICAM-1 and anti-human VCAM-1 antibody, but not by anti-human ELAM-1 antibody. Pretreatment of monocytes with anti-human integrin beta 2 antibody significantly reduced the adhesion of monocytes to IL-1 beta-stimulated SMCs. These results suggest that IL-1 beta is a potent inducer for ICAM-1 and VCAM-1 expression in human vascular SMC, and could play a role in the pathogenesis of atherosclerosis by recruitment and retention of inflammatory cells such as monocytes and neutrophils in the lesions.

Base Sequence↗
PubMed2001

Heterogeneity of smooth muscle cells in advanced human atherosclerotic plaques: intimal smooth muscle cells expressing a fibroblast surface protein are highly activated by platelet-released products.

BACKGROUND: In vascular disease, smooth muscle cells (SMC) undergo phenotypic modulation and may acquire properties resembling those of fibroblasts in tissue wound healing. AIMS: We aimed to show the differential expression of a fibroblast surface protein (FSP) by SMC in atherosclerotic lesions. RESULTS: In early human coronary atherosclerotic lesions the expression of FSP in the intima was absent. In contrast, 29 of 29 middle/advanced lesions contained intimal SMC expressing high levels of FSP. Fibroblast surface protein positive SMC were negative for desmin but expressed variable levels of alpha-SM actin, SM caldesmon, SM myosin heavy chain and vimentin. Explants from advanced atherosclerotic lesions yielded two main SMC subpopulations. SMC over-expressing FSP exhibited higher in vitro mitogenic response (premitotic DNA synthesis) to sera (2- to 8-fold) and platelet-released products (8- to 26-fold), especially from thrombin-activated platelets, than FSP-negative SMC. CONCLUSIONS: Our results suggest that the expression of FSP in SMC could indicate an activated phenotype, and the presence of highly positive FSP cells in the atherosclerotic lesions might be indicative of an increased SMC responsiveness to processes that locally generate thrombin and activate platelets.

Animals↗
PubMed2002

Effects of nitric oxide donors on vascular smooth muscles depend on a type of vascular smooth-muscle preactivation.

The abilities of such therapeutic nitrovasodilators as sodium nitroprusside (SNP) and glyceryl trinitrate (GTN) to dilate vascular smooth muscles (VSM) and affect intracellular calcium concentration level ([Ca2+]i) in a rat tail artery were tested under different types of preactivation. To shed light on mechanisms underlying possible differences in the action of these two nitric oxide (NO) donors, simultaneous measurements of [Ca2+]i and contractile force were done. All vascular rings were precontracted either using a high-K+-Krebs solution or phenylephrine (PE). It was shown that the effect of both NO donors strongly depended on a type of VSM preactivation. The EC50 for GTN under K+ stimulation of VSM comprised (2.48 +/- 1.6) x 10(-5) M, whereas the mean EC50 under PE stimulation was (3.05 +/- 2.3) x 10(-4) M (p < 0.05, n = 9). The EC50 for SNP under K+ stimulation of VSM comprised (1.09 +/- 0.47) x 10(-7) M, whereas the EC(50) under PE stimulation was (8.01 +/- 2.4) x 10(-6) M (p < 0.05, n = 9). GTN demonstrated a significant discrepancy in the magnitude of changes in [Ca2+]i and related VSM relaxant responses, indicating the ability of GTN to relax VSM in the absence of a proportional decrease in [Ca2+]i. The main peculiarity of SNP action under K+ stimulation as compared to PE stimulation was the transient decrease in [Ca2+]i while relaxation was sustained. Therefore, both NO donors demonstrated their ability to produce vasorelaxation as a result of an alteration in myofilament calcium sensitivity. These data clearly indicate that the sensitivity of VSM to NO donors is higher under K+ depolarization than that seen under PE stimulation, indicating that Ca2+ entry through voltage-operated calcium channels is more sensitive to NO as compared to calcium mobilization by means of Ca2+ entry through receptor- operated calcium channels or intracellular Ca2+ release, or both.

Animals↗
PubMed1980

Effects of nonspecific smooth muscle relaxants on tissue concentrations of high energy phosphates and mechanical activity of normal polarized and depolarized intestinal smooth muscles from guinea pig.

Effects of nonspecific smooth muscle relaxants, an uncoupler and removal of Ca ions from physiological solution on the tissue concentrations of high energy phosphates, such as ATP and creatine phosphate (CP) and tension of the normal polarized and KCl-depolarized intestinal smooth muscles of guinea pig were studied. Decrease of CP-concentration induced by dinitrophenol (DNP; 10(-4) M) was accompanied by relaxation of the normal polarized and KCl-depolarized smooth muscles. DNP slightly (but significantly) decreased ATP-concentration in the normal polarized and KCl-depolarized smooth muscles. Application of papaverine ( 3 x 10(-5) M) relaxed the normal polarized taenia immediately but increased CP-concentration at 5 and 10 min and decreased the concentration at 20 min. When the depolarized smooth muscle was considerably relaxed by papaverine (3 x 10(10-5) M), there was little influence on the CP-concentration. After relaxation of the depolarized taenia as induced by papaverine had reached a maximal amplitude, CP-concentration decreased significantly. ATP-concentration was little influenced by papaverine in the normal polarized and KCl-depolarized muscles. Although the treatments with a synthetic antispasmodic drug, Aspaminol (3 x 10(-4) M), which was found to inhibit Ca-uptake by the intestinal smooth muscles, a Ca-blocker, D-600 (10(-6) M) and removal of Ca ions from physiological solution relaxed the polarized and depolarized smooth muscles, the tissue concentrations of CP and ATP increased. These phenomena are considered to be due to decrease of the intracellular Ca-concentration.

Adenosine Triphosphate↗
PubMed2007

Amniotic fluid and bone marrow derived mesenchymal stem cells can be converted to smooth muscle cells in the cryo-injured rat bladder and prevent compensatory hypertrophy of surviving smooth muscle cells.

PURPOSE: Wound healing of the cryo-injured bladder can bring about organ remodeling because of incomplete reconstitution of depleted smooth muscle cells. Stem cell transplantation could be beneficial to improve smooth muscle cell regeneration and/or modulate the remodeling process. The repair of bladder injury using adult-type stem cells would be useful for adult urological patients but unsuited for neonatal patients, in whom major benefits are likely to derive from fetal-type stem cells. MATERIALS AND METHODS: The smooth muscle cell differentiation potential of fetal-type vs adult-type stem cells was evaluated by injecting green fluorescent protein labeled mesenchymal stem cells from rat amniotic fluid or bone marrow, respectively, in cryo-injured rat bladder walls. RESULTS: At 30 days after transplantation only a few fetal-type or adult-type mesenchymal stem cells gave rise to enteric or vascular smooth muscle cells, whereas most mesenchymal stem cells appeared incapable of specific differentiation. In vitro co-culture experiments of smooth muscle cells with fetal-type or adult-type mesenchymal stem cells selectively labeled with distinct fluorochromes showed the presence of hybrid cells, suggesting that some mesenchymal stem cells can undergo cell fusion. Surprisingly the major effect of rat bone marrow or amniotic fluid mesenchymal stem cell transplantation seemed to be preventing cryo-injury induced hypertrophy of surviving smooth muscle cells. CONCLUSIONS: In this model stem cell transplantation has a limited effect on smooth muscle cell regeneration. Instead it can regulate post-injury bladder remodeling, possibly via a paracrine mechanism.

Amniotic Fluid↗