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PubMed2004

Factors controlling airway smooth muscle proliferation in asthma.

Airway smooth muscle proliferation has been the focus of considerable attention, as it is a quantitatively important component of the airway wall remodeling response in asthma and has been suggested as a suitable target for the development of novel anti-asthma agents. Such agents are considered likely to reduce airway hyperresponsiveness and, consequently, airway obstruction, resulting in fewer symptoms and exacerbations. Identifying suitable drug targets has proved an elusive goal, as no dominant molecular mechanism for remodeling has emerged. Moreover, recent findings raise some doubt as to whether smooth muscle proliferation per se is the explanation of the increase in smooth muscle cell number in asthma, with alternative explanations including the proposal that cells migrate either from the interstitial compartment or from a circulating precursor stem cell population. Therefore, drug targeting of migration responses should be considered as an alternative approach to regulating the smooth muscle component of airway wall remodeling.

Airway Resistance↗
PubMed1984

Effect of Ca2+-independent myosin light chain kinase on different skinned smooth muscle fibers.

In various skinned smooth muscle fiber preparations, (porcine carotid artery, rat tail artery, chicken gizzard and Taenia coli from guinea pig) a Ca2+-independent myosin light chain kinase (MLCK) initiated a contraction in absence of Ca2+. While the Ca2+ insensitive MLCK was effective on the vertebrate smooth muscles it did not act on the invertebrate skinned skeletal muscle preparation from Limulus and anterior byssus retractor muscle from Mytilus edulis. The results indicate that in vertebrate smooth muscles phosphorylation is sufficient for activation and that there is no obligatory role for an additional mechanism in initiation of contraction.

Adenosine Triphosphate↗
PubMed2002

2-Aminoethoxydiphenyl borate causes dissociation between membrane electrical and mechanical activity in guinea-pig urinary bladder smooth muscle.

Physiological functions of urinary bladder profoundly reflect smooth muscle mechanical activity. Urinary bladder smooth muscle itself produces myogenic rhythmic contraction, and this spontaneous mechanical event could be the fundamental determinant of urinary bladder functions. The spontaneous contraction of urinary bladder smooth muscle is thought to be triggered primarily by the action potential generated in this smooth muscle cell. Modulators of ion channels contributing to the configuration of action potential also affect urinary bladder smooth muscle mechanical activity as expected exactly from the effects on the electrical event. In the present study, we show that the frequency of action potential recorded in intact strip of guinea-pig urinary bladder smooth muscle is dramatically increased by 2-aminoethoxydiphenyl borate (2-APB; 30 microM) from 0.2 Hz to 1 Hz (approximately 500% increments). In contrast to an increasing effect expected from the membrane electrical alterations, mechanical activity (both contraction amplitude and frequency) of this smooth muscle is unexpectedly reduced by the same concentration of 2-APB to approximately 35% of the control. The present results firstly show an apparent dissociation of electrical-mechanical coupling in urinary bladder smooth muscle. The alteration of membrane electrical activity might not be the exclusive trigger mechanism responsible for the generation of spontaneous rhythmic contraction of this smooth muscle.

Action Potentials↗
PubMed1978

Myotonia dystrophica with heart involvement: an electron microscopic study of skeletal, cardiac, and smooth muscle.

The electron microscopic features of the striated skeletal muscle, the striated cardiac muscle, and the smooth muscle from a woman who had been suffering for many years from myotonia dystrophica with cardiac involvement are described. The skeletal muscle was studied at two different stages of the disease. In the first material the main changes consisted of centrally situated nuclei, disorganisation of the sarcomeres, and focal disruption of the Z-line. The satellite cells were well represented. Three years later atrophy and degenerative, necrotic changes of the skeletal muscle were evident. The satellite cells were absent. Few changes were seen in the striated cardiac muscle. These consisted of slight interstitial fibrosis and large accumulations of mitochondria with intramitochondrial dense granules. The smooth muscle cells of the oesophagus showed disorientated filaments and mild degenerative changes. It is concluded that the skeletal muscle was more severely affected than the other types of muscle.

Aorta↗
PubMed2000

Human malignant melanoma cells release a factor that inhibits the expression of smooth muscle alpha-actin.

Smooth muscle alpha-actin (SMA) is a cytoskeletal protein expressed in vascular smooth muscle cells, pericytes, hair follicle dermal sheaths and myofibroblasts which appear in the process of wound healing and tumor growth. To examine the effect of malignant melanoma on the expression of SMA in these non-neoplastic cells, we carried out immunohistochemical staining and a cell culture study. Conditioned medium prepared from a melanoma cell line M14 was incubated with a rat fibroblastic cell line 3Y1, which had been shown to express SMA. Human cells that had migrated from nevus tissue were also cultured either with or without M14 conditioned medium. Immuno-histochemical staining of human melanoma tissues suggested that the expression of SMA was low in the vicinity of the tumor as well as within the tumor nodules. The conditioned medium from melanoma, but not the medium from control non-neoplastic cells, suppressed the expression of SMA both in the 3Y1 cells and human cells that migrated from the nevus. Preincubation of the medium with anti-platelet-derived growth factor allowed 76% recovery of SMA expression. These data thus imply that melanoma cells release a platelet-derived growth factor-like substance which has a suppressive effect on the contractile elements in non-neoplastic cells.

Actins↗
PubMed1993

Basic fibroblast growth factor has a differential effect on MyoD conversion of cultured aortic smooth muscle cells from newborn and adult rats.

MyoD is a master regulatory gene for myogenesis that also converts many mesoderm-derived cells into the skeletal muscle phenotype. Rat aortic smooth muscle cells do not contain MyoD homologous mRNA. However, expression of an exogenously supplied MyoD gene in aortic smooth muscle cells cultured from newborn and adult animals converts these cells to elongated myoblasts and myotubes expressing the skeletal muscle genes for titin, nebulin, myosin, and skeletal alpha-actin. The presence of basic fibroblast growth factor during growth and serum starvation completely inhibits MyoD-mediated conversion in cultures of newborn smooth muscle cells. However, in smooth muscle cell cultures derived from adult rats the presence of fibroblast growth factor increases the conversion frequency. The differential response of exogenous MyoD suggests that the two morphological types of aortic smooth muscle cells, one typical for the newborn rat, the other for the adult rat, represent two distinctive states of differentiation.

Aging↗
PubMed1997

Effects of protein kinase C alpha overexpression on A7r5 smooth muscle cell proliferation and differentiation.

Smooth muscle cell differentiation and proliferation are increasingly seen to be intimately tied to the etiology of atherosclerosis and hypertension. To determine the role of PKC alpha in the regulation of smooth muscle cell differentiation and proliferation, the rat embryonic smooth muscle cell line A7r5 was transfected with an expression vector containing the full-length PKC alpha cDNA. Neomycin-resistant clones which exhibited increased PKC alpha levels compared to wild-type cells were selected. The A7r5 cells overexpressing PKC alpha had altered morphology and decreased growth rates compared to wild-type cells and cells transfected only with the neomycin resistance gene. Electrophoretic mobility shift assays showed that nuclear extracts from overexpressing clones gave a different pattern of protein-DNA binding to an AP-1 consensus oligonucleotide compared to wild-type cells. In contrast to the growth characteristics of these clones, their levels of cell differentiation marker proteins such as vinculin and desmin were not affected by PKC alpha overexpression. Moreover, the smooth muscle-specific differentiation marker alpha-actin was markedly reduced, while beta-actin levels were found to remain unchanged. Northern blot analysis confirmed that alpha-actin downregulation occurred at the RNA level. Western blot analysis revealed that A7r5 cells have five different PKC isoforms and that these isoform protein levels were not changed by PKC alpha overexpression. These findings suggest that PKC alpha regulates growth and differentiation of A7r5 smooth muscle cells and that these changes might result from altered expression/function of AP-1 transcription factors.

Actins↗
PubMed2005

Receptor-operated Ca2+ entry mediated by TRPC3/TRPC6 proteins in rat prostate smooth muscle (PS1) cell line.

Prostate smooth muscle cells predominantly express alpha1-adrenoceptors (alpha1-AR). alpha1-AR antagonists induce prostate smooth muscle relaxation and therefore they are useful therapeutic compounds for the treatment of benign prostatic hyperplasia symptoms. However, the Ca(2+) entry pathways associated with the activation of alpha1-AR in the prostate have yet to be elucidated. In many cell types, mammalian homologues of transient receptor potential (TRP) genes, first identified in Drosophila, encode TRPC (canonical TRP) proteins. They function as receptor-operated channels (ROCs) which are involved in various physiological processes such as contraction, proliferation, apoptosis, and differentiation. To date, the expression and function of TRPC channels have not been studied in prostate smooth muscle. In fura-2 loaded PS1 (a prostate smooth muscle cell line) which express endogenous alpha1A-ARs, alpha-agonists epinephrine (EPI), and phenylephrine (PHE) induced Ca(2+) influx which depended on the extracellular Ca(2+) and PLC activation but was independent of PKC activation. Thus, we have tested two membrane-permeable analogues of diacylglycerol (DAG), oleoyl-acyl-sn-glycerol (OAG) and 1,2-dioctanoyl-sn-glycerol (DOG). They initiated Ca(2+) influx whose properties were similar to those induced by the alpha-agonists. Sensitivity to 2-aminoethyl diphenylborate (2-APB), SKF-96365 and flufenamate implies that Ca(2+)-permeable channels mediated both alpha-agonist- and OAG-evoked Ca(2+) influx. Following the sarcoplasmic reticulum (SR) Ca(2+) store depletion by thapsigargin (Tg), a SERCA inhibitor, OAG and PHE were both still able to activate Ca(2+) influx. However, OAG failed to enhance Ca(2+) influx when added in the presence of an alpha-agonist. RT-PCR and Western blotting performed on PS1 cells revealed the presence of mRNAs and the corresponding TRPC3 and TRPC6 proteins. Experiments using an antisense strategy showed that both alpha-agonist- and OAG-induced Ca(2+) influx required TRPC3 and TRPC6, whereas the Tg-activated ("capacitative") Ca(2+) entry involved only TRPC3 encoded protein. It may be thus concluded that PS1 cells express TRPC3 and TRPC6 proteins which function as receptor- and store-operated Ca(2+) entry pathways.

Adrenergic alpha-Agonists↗
PubMed1998

Transforming growth factor beta1 involvement in the conversion of fibroblasts to smooth muscle cells in the rabbit bladder serosa.

In an attempt to identify the growth factors or cytokines involved in the serosal thickening that occurs in rabbit bladder subjected to partial outflow obstruction, the following growth factors--transforming growth factor beta1, platelet-derived growth factor, epidermal growth factor, granulocyte colony-stimulating factor and granulocyte-monocyte colony-stimulating factor--were delivered separately onto the serosal surface of the intact bladder via osmotic minipumps. The proliferative/differentiative cellular response of the rabbit bladder wall was evaluated by bromodeoxyuridine incorporation and immunofluorescence staining with a panel of monoclonal antibodies to cytoskeletal proteins (desmin, vimentin, keratins 8 and 18 and non-muscle myosin) and to smooth muscle (alpha-actin, myosin and SM22) proteins. Administration of the transforming growth factor, but not of the other growth factors/cytokines, was effective in inducing serosal thickening. Accumulating cells in this tissue were identified as myofibroblasts, i.e. cells showing a mixed fibroblast-smooth muscle cell differentiation profile. The phenotypic pattern of myofibroblasts changed in a time-dependent manner: 21 days after the growth factor delivery, small bundles of smooth muscle cells were found admixed with myofibroblasts, as occurs in the obstructed bladder. These 'ectopic' muscle structures displayed a variable proliferating activity and expressed an immature smooth muscle cell phenotype. The complete cellular conversion to smooth muscle cells was not achieved if transforming growth factor beta1 was delivered to fibroblasts of subcutaneous tissue. These findings suggest a tissue-specific role for this growth factor in the cellular conversion from myofibroblast to smooth muscle cells.

Animals↗
PubMed1995

[Neural control of tracheal smooth muscle during cough].

Contraction of tracheal smooth muscle during mechanically induced coughing was studied in dogs. Recordings of smooth muscle tension were obtained from the cervical trachea, which is not influenced by intrathoracic pressure. We observed that during breathing at rest, tracheal smooth muscle contracts and relaxes in synchrony with phrenic nerve activity. When cough occurs, the tracheal smooth muscle contracts continuously and tonically with no rhythmic correlation to phrenic nerve activity. Sometimes the contraction starts before the phrenic nerve activity increases. A neuromuscular blocking agent caused a significant decrease in phrenic nerve activity in response to mechanical stimulation. The correlation between phrenic nerve activity and tracheal smooth muscle tension during normal breathing was also observed after afferent inputs from pulmonary mechanoreceptors were interrupted. During coughing, however, this correlation was lost. From these results we conclude that the neural control of tracheal smooth muscle is at least partially independent of phrenic nerve activity during coughing. Because coughing was attenuated by neuromuscular blocking agents, we speculate that there is a positive feedback mechanism from receptors in the chest wall or airway, which increases the magnitude of coughing.

Animals↗