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PubMed1992

Fast Na+ channels and slow Ca2+ current in smooth muscle from pregnant rat uterus.

Smooth muscle cells normally do not possess fast Na+ channels, but inward current is carried through two types of Ca2+ channels: slow (L-type) Ca2+ channels and fast (T-type) Ca2+ channels. Using whole-cell voltage clamp of single smooth muscle cells isolated from the longitudinal layer of 18-day pregnant rat uterus, depolarizing pulses, applied from a holding potential of -90 mV, evoked two types of inward current, fast and slow [8]. The fast inward current decayed within 30 ms, depended on [Na]o, and was inhibited by TTX (K0.5 = 27 nM). The slow inward current decayed slowly, was dependent on [Ca]o, and was inhibited by nifedipine. These results suggest that the fast inward current is a fast Na+ channel current, and that the slow inward current is a Ca2+ slow channel current. A fast-inactivating Ca2+ channel current was not evident. Thus, the ion channels which generate inward currents in pregnant rat uterine cells are TTX-sensitive fast Na+ channels and dihydropyridine-sensitive slow Ca2+ channels. The number of fast Na+ channels increased during gestation. The averaged current density increased from 0 on day 5, to 0.19 on day 9, to 0.56 on day 14, to 0.90 on day 18, and to 0.86 pA/pF on day 21. This almost linear increase occurs because of an increase in the fraction of cells which possess fast Na+ channels, and it is suggested that the fast Na+ current may be involved in spread of excitation. The Ca2+ channel current density also was higher during the latter half of gestation. These results indicate that the fast Na+ channels and Ca2+ slow channels in myometrium become more numerous as term approaches, and may facilitate parturition. Isoproterenol (beta-agonist) did not affect either ICa(s) or INa(f), whereas Mg2+ (K0.5 of 12 mM) and nifedipine (K0.5 of 3.3 nM) depressed ICa(s). Oxytocin had no effect on INa(f) and actually depressed ICa(s) to a small extent. Therefore, the tocolytic action of beta-agonists cannot be explained by an inhibition of ICa(s), whereas that of Mg2+ can be so explained. The stimulating action of oxytocin on uterine contractions is not due to stimulation of ICa(s). Figure 11 summarizes the possible mechanisms by which uterine contractility can be modulated. In contrast to vascular smooth muscle, neither ISO nor adenosine, which produce elevation of cyclic AMP, affected ICa and INa. Therefore, no arrow can be drawn between cA-PK/cG-PK and the Ca2+ slow channel.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine↗
PubMed1999

Long-term effects of Ca(2+) on structure and contractility of vascular smooth muscle.

Culture of dispersed smooth muscle cells is known to cause rapid modulation from the contractile to the synthetic cellular phenotype. However, organ culture of smooth muscle tissue, with maintained extracellular matrix and cell-cell contacts, may facilitate maintenance of the contractile phenotype. To test the influence of culture conditions, structural, functional, and biochemical properties of rat tail arterial rings were investigated after culture. Rings were cultured for 4 days in the absence and presence of 10% FCS and then mounted for physiological experiments. Intracellular Ca(2+) concentration ([Ca(2+)](i)) after stimulation with norepinephrine was similar in rings cultured with and without FCS, whereas force development after FCS was decreased by >50%. The difference persisted after permeabilization with beta-escin. These effects were associated with the presence of vasoconstrictors in FCS and were dissociated from its growth-stimulatory action. FCS treatment increased lactate production but did not affect ATP, ADP, or AMP contents. The contents of actin and myosin were decreased by culture but similar for all culture conditions. There was no effect of FCS on calponin contents or myosin SM1/SM2 isoform composition, nor was there any appearance of nonmuscle myosin. FCS-stimulated rings showed evidence of cell degeneration not found after culture without FCS or with FCS + verapamil (1 microM) to lower [Ca(2+)](i). The decreased force-generating ability after culture with FCS is thus associated with increased [Ca(2+)](i) during culture and not primarily caused by growth-associated modulation of cells from the contractile to the synthetic phenotype.

Animals↗
PubMed1986

Isolated smooth muscle cells preparation.

Detached smooth muscle cells from rat gastric antrum were isolated by incubation with collagenase and examined for viability and motility. Each stomach yielded about 10(7) muscle cells and were judged as intact and viable by the trypan blue dye exclusion. It is concluded that isolated smooth muscle cells of the rat gastric antrum by the technique of incubation with collagenase are judged viable and suitable for characterization of receptors on the surface membranes of these cells.

Animals↗
PubMed2000

Transforming growth factor-beta is an autocrine mitogen for a novel androgen-responsive murine prostatic smooth muscle cell line, PSMC1.

A prostatic smooth muscle cell line (PSMC1) was established from the dorsolateral prostate of p53 null mice. The cell line is nontumorigenic when inoculated subcutaneously, under the renal capsule or intraprostatically in syngeneic mice. These cells express alpha-smooth muscle actin (alpha-SMA), indicating their smooth muscle origin, and TGF-beta significantly enhances expression of alpha-SMA. The cells express both androgen receptor (AR) mRNA and protein, and respond mitogenically to physiological concentrations of androgens. PSMC1 cells produce significant amounts of TGF-beta, which stimulates growth by an autocrine mechanism. Dihydrotestosterone (DHT) increases proliferation of PSMC1 cells by promoting TGF-beta secretion. Considering the significant inhibitory effect of TGF-beta on prostatic epithelial cells and its stimulatory effect on the PSMC1 cells, we postulate that TGF-beta produced by prostatic smooth muscle cells may have a paracrine effect on the prostatic epithelium. We also postulate that TGF-beta may be involved in the etiology of benign prostatic hyperplasia (BPH) by stimulating excessive stromal proliferation. Line PSMC1 is the first reported androgen-responsive murine smooth muscle cell line. It will be useful for in vivo and in vitro experiments to study the mechanisms of androgen action on prostatic stroma and for delineating the interactions that occur between prostatic smooth muscle and epithelium that may lead to prostatic diseases such as BPH.

Androgens↗
PubMed1999

Congenital smooth muscle hamartoma of the conjunctival fornix.

PURPOSE: Congenital smooth muscle hamartomas are benign tumors composed of proliferating smooth muscle cells. They are usually seen as abnormal patches of skin. Ocular involvement of congenital smooth muscle hamartomas is unusual, with rare reports of patients with external eyelid involvement or proptosis resulting from orbital tumors. We describe a patient with a congenital smooth muscle hamartoma that involved the tarsal conjunctival fornix. METHODS: Review of the patient's medical records, including the results of ophthalmologic, radiologic, and histologic examinations. RESULTS: A healthy 2-year-old boy was initially seen with a conjunctival mass. He had a discrete, gray, cystic-appearing lesion in the inferior fornix of the left eye. A magnetic resonance imaging study revealed no signs of extension of the lesion into the orbit. The lesion was surgically excised. Histologic sections showed large bundles of smooth muscle with a fibrotic background and interdigitating fat, consistent with a diagnosis of a congenital smooth muscle hamartoma. CONCLUSION: To our knowledge, this is the first report of a patient with a congenital smooth muscle hamartoma arising from the conjunctival fornix. It presumably originated from either the smooth muscle of the vascular endothelium or from the capsulopapebral muscle. Congenital smooth muscle hamartoma should be considered in the differential diagnosis of cystic-appearing conjunctival fornix lesions.

Child, Preschool↗
PubMed1989

Streaming potential measurements in Ca2+-activated K+ channels from skeletal and smooth muscle. Coupling of ion and water fluxes.

Streaming potentials arising across large-conductance Ca2+-activated K+ channels incorporated into planar lipid bilayers were measured. Ca2+-activated channels obtained either from skeletal muscle or from smooth muscle membranes were used. Streaming potentials were extracted from the current-voltage relationship for the open channel obtained in the presence of an osmotic gradient. The osmotic gradient was established by adding glucose to one side of the membrane. At 300 mM KCl, the average streaming potential was 0.72 mV/osmol per kg for t-tubule channels and 0.83 mV/osmol per kg for smooth muscle channels. Streaming potential values depend on KCl concentration, they decrease as KCl concentration increases, and the value obtained by extrapolation to zero KCl concentration is 0.85 mV/osmol per kg. Assuming that water and ions cannot pass each other, at least in a region of the channel, the streaming potential values obtained indicate that this region contains a minimum of two and a maximum of four water molecules. It is concluded that the channel has a narrow region with a length of 0.6-1.2 nm.

Animals↗
PubMed2001

Vascular endothelial growth factor promotes proliferation and migration of cavernous smooth muscle cells.

PURPOSE: We investigated whether cavernous smooth muscle cells secrete vascular endothelial growth factor (VEGF), how they respond to VEGF and how age affects their ability to secrete and respond to VEGF. MATERIALS AND METHODS: Corpus cavernous tissues were isolated from rats of various ages and grown as monolayer cell cultures. Smooth muscle identity was determined by immunofluorescence staining. Secreted VEGF was measured with a VEGF enzyme-linked immunosorbent assay kit. Cell proliferation was assayed with a cell titer kit. Cell migration was measured with Transwell chambers. VEGF receptor (VEGFR) messenger RNA and proteins were identified by reverse transcription-polymerase chain reaction and immunoblotting, respectively. RESULTS: Cavernous smooth muscle cells from young (age 1 week) and old (age 28 months) rats secreted the least amounts of VEGF and those from 16-week-old rats secreted the most. VEGF stimulated the growth of cavernous smooth muscle cells at an optimal concentration of 12.5 ng./ml. At this concentration cavernous smooth muscle cells from 11-week-old and 28-month-old rats showed the highest and lowest growth rates, respectively. The optimal VEGF concentration for cavernous smooth muscle cell migration was 10 ng./ml. At this concentration cells from 4-week-old and 28-month-old rats showed the highest and lowest migratory rates, respectively. The expression of VEGFR-1 appeared to parallel the VEGF regulated growth rates of these cells. VEGFR-2 was undetectable in cavernous smooth muscle cells. CONCLUSIONS: Cavernous smooth muscle cells from rats of different ages secreted different amounts of VEGF and showed different abilities to respond to VEGF. Cavernous smooth muscle cells responded to VEGF in terms of cell proliferation and migration. Cavernous smooth muscle cells from rats of different ages expressed different levels of VEGFR-1 but did not express VEGFR-2.

Aging↗
PubMed1995

Characterization of Ca2+/calmodulin-dependent protein kinase II from smooth muscle.

We have characterized chicken gizzard smooth muscle Ca2+/calmodulin-dependent protein kinase II (CaM-PKII) with particular focus on its autophosphorylation. The autophosphorylation of smooth muscle CaMPKII produced a partially constitutively active enzyme, as occurs with the alpha- and beta-isoforms of this enzyme, but the autophosphorylation kinetics were significantly slower. Phosphorylation during the initial rapid phase coincided with the production of constitutively active enzyme. The phosphorylation was on both serine and threonine residues, which is distinct from the brain enzyme where threonine phosphorylation is much faster and more prevalent than serine phosphorylation. The major autophosphorylation sites identified were different from the known autophosphorylation sites of the alpha- and beta-isoforms. During the initial autophosphorylation phase Ser-319, Ser-352 and a Thr residue within residues 345-368 were found to be phosphorylated. During the subsequent gradual phase two serine residues in the variable region and Ser-280 were phosphorylated, but Thr-286 and Thr-305, which are the known major autophosphorylation sites for the alpha- and beta-isoforms, were not detected as the major autophosphorylation sites of smooth muscle CaMPKII. By comparing the phosphopeptide sequence with the known sequences of various isoforms, we concluded that isoform gamma-b, which contains a unique insertion and two deletions at the C-terminal side of the calmodulin binding domain, is the dominant CaMPKII isoform in smooth muscle. The molecular mass of smooth muscle CaMPKII was estimated to be 240 kDa which would comprise four subunits, fewer than in the alpha- and beta-isoforms. The results show that smooth muscle CaMPKII is functionally distinct from the alpha- and beta-isoforms of this enzyme, which might be crucial for its physiological relevance.

Amino Acid Sequence↗
PubMed1992

Expression of M-CSF receptor encoded by c-fms on smooth muscle cells derived from arteriosclerotic lesion.

Vascular smooth muscle cells in atherosclerotic lesions are phenotypically different from those in the normal arterial wall, and no expression of macrophage colony stimulating factor (M-CSF) receptor encoded by the proto-oncogene c-fms has been demonstrated in normal smooth muscle cells. In the present study, we demonstrated expression of c-fms and high affinity binding of M-CSF in smooth muscle cells isolated from an experimental rabbit model of arteriosclerosis (intimal smooth muscle cells), while no expression of c-fms was shown in medial smooth muscle cells. In the immunocytochemical analysis, both types of smooth muscle cells similarly reacted with an antibody specific to muscle cells (HHF 35) but did not react with an antibody specific to rabbit macrophages (RAM 11). In intimal smooth muscle cells, when cells were incubated with acetylated low density lipoproteins (LDL), the binding of acetylated LDL and foam cell formation were observed. In response to M-CSF, tyrosine-phosphorylation, as analyzed by the detection of anti-phosphotyrosine-reactive proteins, and an increased rate of cell proliferation were observed in intimal smooth muscle cells. These results indicated that intimal smooth muscle cells have the characteristics of monocyte-macrophages such as the expression of c-fms, which may be related to their proliferation and phenotypic conversion into foam cells in atheromatous lesions.

Animals↗
PubMed2003

Molecular basis and characteristics of KATP channel in human corporal smooth muscle cells.

Relaxation of the corpus cavernosum smooth muscle is an absolute prerequisite for penile erection. Potassium channels play a role in the physiologic regulation of corporal smooth muscle tone. In spite of the physiological importance of K(ATP) channel in the modulation of corporal smooth muscle tone, there is a shortage of information available about the K(ATP) channel subtype(s) present in the corporal smooth muscle. The purpose of this study was to investigate the subunit type of K(ATP) channel, that is, the combinations of the Kir subunit and the SUR subunit in the human corporal smooth muscle and determine whether the electrophysiological kinetics and pharmacological properties of K(ATP) channels meet the subunit characteristics of the ion channel. We used cultured human corporal smooth muscle cells. To determine the presence of Kir and SURs subunits, RT-PCR was performed using Kir6.1, Kir6.2, SUR1, SUR2A, and SUR2B gene-specific primers. For electrophysiological recordings, the whole-cell, inside-out, and cell-attached configurations of the patch-clamp technique were used. We observed transcripts for Kir6.1, Kir6.2, and SUR2B in mRNA isolated from smooth muscle cells of cultured human corpus carvernosum. We recorded the unitary K(ATP) channel under the condition of intracellular and extracellular 140 mM [K(+)], and the slope conductance of the channel was 42.0+/-2.6 pS which is an intermediate conductance between that of either Kir6.1 or Kir6.2. The pinacidil (10 microM) increased the magnitude of the outward K(+) current (214.6+/-89.2%, n=12, < or = 0.05), which was blocked by the subsequent addition of the specific K(ATP) channel subtype selective blocker, glibenclamide (10 microM). The SIN-1(200 microM) induced increases in whole-cell outward K(+) currents (126.0+/-1.4%, n=4). The increased currents by SIN-1 were inhibited by glibenclamide (10 microM). We are the first to show that K(ATP) channel in human corporal smooth muscle is composed of Kir6.1-Kir6.2 construct expressed with SUR2B by RT-PCR. These findings, taken together with the electrophysiological results, suggest that K(ATP) channel in corporal smooth muscle cells is composed of heteromultimers of Kir6.1 and Kir6.2 with the ratio of 3 : 1 or 4 : 0 and SUR2B.

ATP-Binding Cassette Transporters↗
PubMed1992

In vivo recording of electrical activity of canine tracheal smooth muscle.

Electrical activity of the tracheal smooth muscle was studied using extracellular bipolar electrodes in 37 decerebrate, paralyzed, and mechanically ventilated dogs. A spontaneous oscillatory potential that consisted of a slow sinusoidal wave of 0.57 +/- 0.13 (SD) Hz mean frequency but lacked a fast spike component was recorded from 15 dogs. Lung collapse accomplished by bilateral pneumothoraxes evoked or augmented the slow potentials that were associated with an increase in tracheal muscle contraction in 26 dogs. This suggests that the inputs from the airway mechanoreceptors reflexly activate the tracheal smooth muscle cells. Bilateral vagal transection abolished both the spontaneous and the reflexly evoked slow waves and provided relaxation of the tracheal smooth muscle. Electrical stimulation of the distal nerve with a train pulse (0.5 ms, 1-30 Hz) evoked slow-wave oscillatory potentials accompanied by a contraction of the tracheal smooth muscle in all the experimental animals. Our observations in this in vivo study confirm that the electrical activity of tracheal smooth muscle consists of slow oscillatory potentials and that tracheal contraction is at least partly coupled to the slow-wave activity of the smooth muscle.

Action Potentials↗
PubMed1997

Mitogen-activated protein kinase activation is involved in platelet-derived growth factor-directed migration by vascular smooth muscle cells.

Migration of vascular smooth muscle cells (VSMCs) is a crucial response to vascular injury resulting in neointima formation and atherosclerosis. Platelet-derived growth factor (PDGF-BB) functions as a potent chemoattractant for VSMCs and enhances these pathologies in the vasculature. However, little is known about the intracellular pathways that mediate VSMC migration. In the present study, we investigated the role of mitogen-activated protein kinase (MAPK) activation in this function, since PDGF-BB as well as other growth factors activate this pathway. Using an in-gel kinase assay, we observed that PD 98059 an inhibitor of MEK that activates MAP kinase, inhibited PDGF-BB-induced activation of ERK-1 and ERK-2 in cultured rat aortic smooth muscle cells in a concentration-dependent manner. In contrast, PDGF-mediated activation of intracellular calcium release was not affected by PD 98059. The chemotactic response of both rat aortic smooth muscle cells (RASMCs) and human umbilical vein smooth muscle cells (HUSMCs) toward PDGF-BB (10 ng/mL) was significantly reduced by PD 98059 (10 mumol/L) to 41.7 +/- 7.1% in RASMCs (P < .01) and to 47.2 +/- 5.3% in HUSMCs (P < .01). Similar inhibition was seen at 30 mumol/L, less at 1 mumol/L. To further confirm the specificity of these results implicating the MAPK pathway, an antisense oligodeoxynucleotide (ODN) directed against the initiation translation site of rat ERK-1 and ERK-2 mRNA was used to suppress MAP kinase synthesis and function in rat VSMCs. Liposomal transfection with 0.4 mumol/L antisense ODN reduced ERK-1 and ERK-2 protein by 65% (P < .01) after 48 hours. The chemotactic response to PDGF-BB (10 ng/mL) was reduced by 75% (P < .01) in rat VSMCs transfected with the same antisense ODN concentration. Sense and scrambled control ODNs (0.4 mumol/L) did not affect ERK-1 and ERK-2 protein concentrations or chemotaxis of VSMCs induced by PDGF-BB. These experiments provide the first evidence that activation of MAPK is a critical event in PDGF-mediated signal transduction regulating VSMC migration.

Animals↗
PubMed1992

Agonist-induced production of inositol phosphates in human airway smooth muscle cells in culture.

Smooth muscle cells (SMC) from human bronchi were isolated by elastase treatment, subcultured, and characterized by their positive reaction with a monoclonal antibody against alpha-smooth muscle actin (alpha SMA). In each cell line tested, at least 95% of the cells were positively stained. The functional properties of these cells were examined by measuring the metabolism of inositol phosphates (IPs). For that purpose, cells were incubated for 3 days before reaching confluency in the presence of myo-[3H]inositol in order to label the phosphoinositide pool, and the various [3H]IPs were separated by HPLC on a SAX column with a phosphate gradient. IP1 isomers were separated in three peaks; IP2, IP3, IP4, IP5 and IP6 (phytic acid) were each eluted as single peaks. The identity of the [3H]peaks was verified with corresponding [3H]IP standards. The accumulation of [3H]IPs was measured by incubating cells up to 30 min in the presence of 10 mM LiCl, with or without a bronchoconstrictor agent (carbachol, histamine, PGF2 alpha). Histamine, 10(-4) M, elicited a four times larger IP accumulation than carbachol, 10(-4) M, and than PGF2 alpha, 5 10(-5) M. Dose-response curves were established for histamine and carbachol in the range 10(-7)-10(-4) M. At 10(-7) M, carbachol was more effective than histamine in stimulating the IP metabolism. Atropine blocked the response to carbachol, and diphenhydramine inhibited the effect of histamine, indicating the specificity of the response to the agonists. These results indicate that cultured human bronchial SMC are a suitable preparation for studying physiological aspects of membrane transduction in the airways.

Bronchi↗
PubMed2004

Smooth muscle stem cells.

Vascular smooth muscle cells (SMCs) originate from multiple types of progenitor cells. In the embryo, the most well studied SMC progenitor is the cardiac neural crest stem cell. Smooth muscle differentiation in the neural crest lineage is controlled by a combination of cell intrinsic factors, including Pax3, Tbx1, FoxC1, and serum response factor, interacting with various extrinsic factors in the local environment such as bone morphogenetic proteins (BMPs), Wnts, endothelin (ET)-1, and FGF8. Additional sources of multipotential cells that give rise to vascular SMCs in the embryo include proepicardial cells and possibly endothelial progenitor cells. In the adult, vascular SMCs must continually repair arterial injuries and maintain functional mass in response to changing demands upon the vessel wall. Recent evidence suggests that this is accomplished, in part, by recruiting multipotential vascular progenitors from bone marrow-derived stem cells as well as from less well defined sources within adult tissues themselves. This article will review our current understanding of the origins of vascular SMCs from multipotential stem and progenitor cells in developing as well as adult vasculature.

Animals↗
PubMed1994

H19, a developmentally regulated gene, is reexpressed in rat vascular smooth muscle cells after injury.

Vascular smooth muscle cell migration, proliferation, and differentiation are central to blood vessel development. Since neointimal formation after vascular injury may require the reexpression of a smooth muscle developmental sequence, we examined the expression of H19, a developmentally regulated gene, in rat blood vessels. Expression of the H19 gene is associated with the differentiation process that takes place during development of many tissues. Consistent with this, H19 was highly expressed in the 1-d-old rat aorta but was undetectable in the adult. H19 transcripts were only minimally detected in uninjured carotid artery but were abundant at 7 and 14 d after injury and were localized by in situ hybridization, primarily to the neointima. H19 transcript were undetectable in proliferating neointimal cells in culture but became highly abundant in postconfluent, differentiated neointimal cells. H19 transcripts were only minimally expressed in adult medial smooth muscle cells grown under the identical conditions. Thus, H19 may play an important role in the normal development and differentiation of the blood vessel and in the phenotypic changes of the smooth muscle cells, which are associated with neointimal lesion formation. The vascular injury model may be a useful system to use in examining the function of H19.

Aging↗
PubMed2003

Strain rate mechanotransduction in aligned human vascular smooth muscle cells.

Vascular smooth muscle cells (VSMCs) exist in a dynamic mechanical environment and can sense and respond to mechanical stimuli in vivo. Stretch is known to stimulate intracellular biochemical events, but the influence of the rate at which stretch is applied has not been extensively investigated. Also, most studies of VSMC mechanotransduction use cell culture models not aligned in the direction of stretch. We aligned human VSMC in the direction of uniaxial stretch to examine the importance of strain rate and cell orientation. We demonstrate strain rate profoundly affects stretch-induced phosphorylation of extracellular signal-regulated kinase (ERK)1/2. Low strain rate induced dephosphorylation while physiologic and high rates increased phosphorylation. Dephosphorylation at low strain rate was dependent on cell orientation matching the strain field. Pretreatment with GDPbetaS indicated G proteins are required for ERK1/2 phosphorylation at physiologic strain rate. Apyrase addition to scavenge extracellular ATP inhibited ERK1/2 regulation at low and physiologic strain rates. These results indicate strain rate and cell orientation are important components of mechanotransduction.

Anisotropy↗
PubMed1988

[Magnesium ions and contractile activity of vascular smooth muscle cells in hypoxia].

In isolated smooth muscle of the rat portal vein removal of Mg2+ from perfusate induced rapid enhancement of frequency and amplitude of spontaneous contractions and decreased inhibiting effect of hypoxia on the smooth muscle contractile activity. Concomitant elevation of extracellular Ca2+ has no additional protective effect on the smooth muscle in hypoxia. Ten-fold lowering of Mg2+ content in buffer solution resulted in a significant rise in the tension of the smooth muscle activated by Ca2+. The data obtained suggest that protective effect of Mg2+-free solution on vascular smooth muscle in hypoxia may be mediated not only through increases intracellular Ca2+ concentration but also due to rising sensitivity of the smooth muscle cells contractile protein to Ca2+.

Animals↗
PubMed2000

Cyclic mechanical strain decreases the DNA synthesis of vascular smooth muscle cells.

In vivo, smooth muscle cells of the vascular wall are rhythmically stretched by the arterial pulse. Here, we test the hypothesis that rhythmical stretch is important for suppressing the growth of vascular smooth muscle (vsm) cells. DNA-synthesis rate, cell number, metabolic activity, and cell death were compared between rhythmically stretched and non-stretched vsm cells from the rat embryonic aortic A10 cell line. Rhythmical stretch (0.5 Hz, 5% elongation, 48 h) did not induce vsm cell proliferation, that is the vsm cell number was constant. Cell damage or necrosis was excluded because the release of lactate dehydrogenase (LDH) was identical. The low rate of apoptosis (0.2%) was not different between stretched cells and control cells. Stretch significantly reduced the DNA-synthesis rate [measured as incorporation of 5-bromo-2'-deoxyuridine (BrdU)] in a time-dependent manner. BrdU incorporation was decreased by 32% after 24 h of cyclic stretching and was further diminished to 50% after 48 h of strain. Metabolic activity (measured by Wst-1 cleavage) was only modestly influenced. The stretch-induced decrease in DNA synthesis was independent of the extracellular matrix. No differences were detected when laminin- or pronectin-coated membranes were used instead of collagen-coated membranes. The effect of stretch was unlikely to be mediated by secretion of an unknown "factor", because vsm cells incubated with medium conditioned by stretched cells did not show a significant decrease in BrdU uptake. The results support the idea that rhythmical stretch is important to keep the rate of DNA synthesis and thereby the proliferation of vsm cells at a low level.

Analysis of Variance↗