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Results for “Phenotypic modulation”

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PubMed1990

[Phenotypic variants of the smooth-muscle cells in an atheromatous plaque of the human aorta].

The authors investigated the expression of cytoskeletal proteins and the ultrastructure of cells in normal intima and atheromatous plaque of human aorta. It has been established, using double immunofluorescent method and a set of antibodies that intimal smooth muscle cells /SMC/ of normal aorta express myosin, vimentin, alpha-actin and actin but not desmin. In seven out of 28 atherosclerotic plaques the cells contained desmin and all other SMC cytoskeletal proteins were found. These cells had the ultrastructural features of SMC, i.e. well-developed endoplasmic reticulum and Golgi apparatus. Besides, some cells in 13 atherosclerotic plaques proved to be myosin-, alpha-actin- and desmin-negative. The cells were stained with monoclonal antibodies specific to SMC but not with macrophage-specific antibody. Ultrastructurally, the cytoplasm of the cells was filled with rough endoplasmic reticulum and a developed Golgi complex, but a certain portion of the cells retained basal lamina and myofilament bundles. The peculiarities of cytoskeletal protein in expression and ultrastructure of cells in human aortic atherosclerotic plaques may be explained by a phenotypic modulation of vascular SMC.

Adolescent↗

PubMed2006

Urokinase plasminogen activator in injured adventitia increases the number of myofibroblasts and augments early proliferation.

Myofibroblasts are involved in vessel remodeling during the development of hypertension as well as after angioplasty and aortocoronary grafting, but the mechanisms of myofibroblastic phenotypic modulation are not fully elucidated. We assessed the role of urokinase plasminogen activator (uPA) and its proteolytic activity in myofibroblast differentiation and the early proliferation following mechanical injury of the rat carotid adventitia. The effects of perivascular application of recombinant uPA (r-uPA), proteolytically inactive r-uPA(H/Q) and uPA neutralizing antibody were evaluated 4 days after surgical injury to the adventitia. The phenotype of adventitial cells was assessed using anti-alpha-smooth muscle actin (alpha-SM actin) antibody, anti-SM heavy chain myosin, anti-high-molecular-weight caldesmon, anti-smoothelin and anti-ED-1 antibodies, proliferation by the expression of proliferating cell nuclear antigen, and the size of the adventitia by quantitative morphometry. Four days after injury, the intensive immunostaining for urokinase appeared in the rat carotid artery adventitia. At the same time, the frequency of alpha-SM actin-positive adventitial cells was 1.8+/-1.1% in uninjured arteries and 25.2+/-5.4% in injured arteries (p<0.05), and the respective frequency of ED-1-positive cells 1.5+/-1.1 and 25.0+/-5.2%. The application of exogenous r-uPA doubled the numbers of alpha-SM actin-positive adventitial cells to 55.7+/-6.8% (p<0.05). ED-1-positive cells and proliferating cell nuclear antigen-positive cells as well as the size of the adventitia were also significantly increased after r-uPA compared with injury alone. In contrast, the proteolytically inactive r-uPA(H/Q) did not affect any parameters. The application of uPA neutralizing antibody attenuated the frequency of alpha-SM actin-positive cells to 12.6+/-3.5% (p<0.05), the frequency of ED-1-positive cells, and the numbers of adventitial cells. r-uPA stimulation of cultured human skin fibroblasts significantly increased the alpha-SM actin content in a concentration-dependent manner. In contrast, r-uPAH/Q did not induce changes in alpha-SM actin content. We conclude that uPA, which is upregulated in the injured adventitia, can augment adventitial cell accumulation, including myofibroblasts, and adventitia growth early after injury of the rat carotid artery adventitia by mechanisms involving proteolysis.

Animals↗

PubMed1989

Phase variation in Bordetella pertussis by frameshift mutation in a gene for a novel two-component system.

Bordetella pertussis, the aetiological agent of whooping cough, coordinately regulates the expression of many virulence-associated determinants, including filamentous haemagglutinin, pertussis toxin, adenylyl cyclase toxin, dermonecrotic toxin and haemolysin. The coordinate regulation is apparent in the repression of synthesis of these determinants in response to environmental stimuli; a phenomenon known as antigenic or phenotypic modulation. B. pertussis also varies between metastable genetic states, or phases. There is a virulent phase in which virulence-associated determinants are synthesized, and an avirulent phase in which they are not. Previous studies have shown that a genetic locus, vir, is required for expression from many virulence-associated loci, and that replacing the cloned vir locus in trans can restore the virulent phase phenotype to spontaneously occurring avirulent phase strains. Here, we show that phase variation in one series of strains is due to a frameshift mutation within an open reading frame that is predicted to code for a Vir protein product. The deduced protein sequence is similar to both components of the 'two-component' regulatory system which control gene expression in response to environmental stimuli in a range of bacterial species.

Base Sequence↗

PubMed2003

Regulation of gene expression by cyclic GMP.

Cyclic GMP, produced in response to nitric oxide and natriuretic peptides, is a key regulator of vascular smooth muscle cell contractility, growth, and differentiation, and is implicated in opposing the pathophysiology of hypertension, cardiac hypertrophy, atherosclerosis, and vascular injury/restenosis. cGMP regulates gene expression both positively and negatively at transcriptional as well as at posttranscriptional levels. cGMP-regulated transcription factors include the cAMP-response element binding protein CREB, the serum response factor SRF, and the nuclear factor of activated T cells NF/AT. cGMP can regulate CREB directly, through phosphorylation by cGMP-dependent protein kinase, or indirectly, through activation of mitogen-activated protein kinase pathways; regulation of SRF and NF/AT by cGMP is indirect, through modulation of RhoA and calcineurin signaling, respectively. Downregulation of the RNA-binding protein HuR by cGMP leads to destabilization of guanylate cyclase mRNA, but this posttranscriptional mechanism may affect many more cGMP-regulated genes. In this review, we discuss the role of cGMP-regulated gene expression in (patho)physiological processes most relevant to the cardiovascular system, such as regulation of vascular tone, cardiac hypertrophy, phenotypic modulation of vascular smooth muscle cells, and regulation of cell proliferation and apoptosis.

Animals↗

PubMed2006

Cell adaptation to a physiologically relevant ECM mimic with different viscoelastic properties.

To successfully induce tissue repair or regeneration in vivo, bioengineered constructs must possess both optimal bioactivity and mechanical strength. This is because cell interaction with the extracellular matrix (ECM) produces two different but concurrent signaling mechanisms: ligation-induced signaling, which depends on ECM biological stimuli, and traction-induced signaling, which depends on ECM mechanical stimuli. In this report, we provide a fundamental understanding of how alterations in mechanical stimuli alone, produced by varying the viscoelastic properties of our bioengineered construct, modulate phenotypic behavior at the whole-cell level. Using a physiologically relevant ECM mimic composed of hyaluronan and fibronectin, we found that adult human dermal fibroblasts modify their mechanical response in order to match substrate stiffness. More specifically, the cells on stiffer substrates had higher modulus and a more stretched and organized actin cytoskeleton (and vice versa), which translated into larger traction forces exerted on the substrate. This modulation of cellular mechanics had contrasting effects on migration and proliferation, where cells migrated faster on softer substrates while proliferating preferentially on the stiffer ones. These findings implicate substrate rigidity as a critical design parameter in the development of bioengineered constructs aimed at eliciting maximal cell and tissue function.

Actins↗

PubMed1993

Regulation of fibroplasia in cutaneous wound repair.

Fibroblast accumulation in a cutaneous wound requires phenotypic modulation of fibroblasts. In response to injury, resident fibroblasts in the surrounding tissue proliferate for the first 3 days and then at day 4 migrate into the wounded site. Once within the wound, they produce type I procollagen as well as other matrix molecules and deposit these extracellular matrix molecules in the local milieu. By day 7, abundant extracellular matrix has accumulated and fibroblasts switch to a myofibroblast phenotype replete with actin bundles along the cytoplasmic face of the plasma membrane. Wound contraction occurs as these myofibroblast gather in the wound extracellular matrix by extending pseudopodia, attaching to extracellular matrix molecules, such as fibronectin and collagen, then retracting the pseudopodia. Once these processes have been accomplished, the fibroblasts appear to undergo apoptosis. Therefore, during cutaneous wound repair, fibroblasts appear to progress through four phenotypes: first proliferating, second migrating, third synthesizing extracellular matrix molecules, and fourth expressing thick actin bundles as myofibroblasts.

Animals↗

PubMed1987

Studies on aorta during development. I. Fetal rabbit aorta under ex vivo and in vitro conditions: rapid changes in smooth muscle cell phenotype, cell proliferation and cholesterol content with organ culture.

The structural development of the already well defined fetal rabbit aortic wall from 22 to 31 days of gestation in vivo consists of increasing aortic wall thickness, elastic lamina continuities, extracellular matrix deposition, and maturing of the fine structure of the medial smooth muscle cells. In vivo at term (31 days), the mature aortic smooth muscle cells demonstrated the characteristic thin, thick and intermediate filaments, dense plaques, endoplasmic reticulum, golgi, plasmalemma vesicles and an incomplete basal lamina. The fetal aorta rapidly responded to organ culture with various changes. Fetal smooth muscle cells modified their phenotype to the synthetic state when cultured in both serum-supplemented and serum-free media. This smooth muscle cell modification occurred after 3 days of culture in fetal explants. The synthetic type smooth muscle cells (fetal) began to proliferate after 6 days of culture. This proliferation resulted in a peripheral outgrowth after 9 days of 10-20 layers in fetal cultures from serum-supplemented media and of 2-4 layers in serum-free media. The orderly arrangement of the internal elastic lamina and alternating medial layers of smooth muscle cells and elastic lamina seen in vivo was disrupted along with increased matrix after 9 days of fetal explant culture. Significant numbers of 'modified' synthetic phenotype smooth muscle cells were not observed in adult aortic explants until after 15 days in culture in serum supplemented media. The mature contractile phenotype smooth muscle cell predominated in adult explants cultured in serum-free media. Significant synthetic phenotype smooth muscle cell proliferation only occurred in adult explants after 15 days culture in serum-supplemented media. When compared to aorta in vivo evidence for increases in cholesterol esterification were observed in both fetal (9 days) and adult (15 days) explants cultured in both serum-supplemented and serum-free media. The fetal aorta in organ culture appeared to be more susceptible than the adult aorta to (a) phenotypic modulation of smooth muscle cells to the synthetic state, (b) smooth muscle cell proliferation, and (c) early cholesteryl ester accumulation.

Aging↗

PubMed2004

Implication of Reg I in human pancreatic duct-like cells in vivo in the pathological pancreas and in vitro during exocrine dedifferentiation.

A feature associated frequently with the pathologic pancreas is the presence of tubular complexes produced by a phenotypic modulation of acinar cells that take on the characteristics of ductular cells. Since the type I Reg gene, an acinar cell product, is increased in the pancreas following an acinar injury, we aimed to evaluate whether the Reg I protein might be involved in this dedifferentiation process in the human pancreas. We studied duct-like structures in fixed human pathologic pancreatic tissues and human cells with a ductal phenotype obtained by culturing human exocrine preparations. Immunocytochemistry, Western blotting, and RT-PCR were applied for detection of type I Reg. Reg I was observed not only in acinar cells but also in the duct-like cells and dilated duct cells, both positive for cytokeratin 19. However, none of the other acinar markers was observed in these cells. In vitro, human acinar cells dedifferentiated, losing their acinar phenotype, but expression of Reg I remained constant throughout the culture duration. Furthermore, Reg I was not associated with proliferation. We demonstrated that Reg I expression was linked to acinar cell dedifferentiation. We postulate that Reg I might be used as a marker to understand the events leading to phenotypic changes of acinar cells to address the physiological role of Reg I in the pancreas.

Adolescent↗

PubMed1991

Isolation and characterization of Bordetella avium phase variants.

Two spontaneous phase variants of Bordetella avium were isolated at a frequency of 2 x 10(-4) by colony immunoblot assay of B. avium with antibody against B. avium dermonecrotic toxin. The two phase variants, designated GOBL309 and GOBL312, lack dermonecrotic toxin and four outer membrane proteins with molecular masses of 93, 48, 38, and 27 kDa but retain the ability to agglutinate guinea pig erythrocytes. The proteins which are not expressed by GOBL309 and GOBL312 correspond to five proteins which are phenotypically modulated in B. avium by growth in the presence of nicotinic acid or MgSO4. Growth of the phase variants in supplemented Stainer-Scholte media containing nicotinamide did not alter expression of these five proteins. Intranasal inoculation of the spontaneous phase variants into 3-day-old turkeys and reisolation of B. avium at 2 weeks postinoculation resulted in the recovery of B. avium which had the wild-type phenotype, colonized the turkey tracheas, and produced the four outer membrane proteins and dermonecrotic toxin. Hybridization of B. avium and B. avium-like chromosomal DNA with internal portions of the Bordetella pertussis virulence regulatory genes, bvgA and bvgS, revealed that B. avium and B. avium-like isolates contain 5.3- and 5.7-kb DNA fragments, respectively, which are homologous to bvgS. B. avium and B. avium-like chromosomal DNA failed to hybridize to B. pertussis bvgA.

Animals↗

PubMedDate not supplied

[The phenotypes of arterial smooth-muscle cells during ontogeny and in atherosclerotic plaques].

Smooth-muscle cell (SMC) myosin expression, SMC alpha-actin, h-caldesmon and calponin expression were studied in developing SMC of embryonic aorta as well as in adult human aorta and coronary arteries. It was found that ontogenesis is associated with SMC phenotypic modulations. In 8-23-week embryos SMC express SMC myosin and alpha-actin. In adult humans arterial SMC express all the markers studied. Normal subendothelium contains a heterogeneous SMC population. SMC heterogeneity is most marked in atherosclerotic plaques in the form of clusters of homogeneous cells different by expression of contractile system proteins. It is suggested that SMC heterogeneous population in atherosclerotic plaques may arise due to proliferation of phenotypically different precursors cells.

Adult↗

PubMed1987

Relationship of human cord blood mononuclear cell lines, established by the HTLV-I integration, to expression of T-cell phenotypes and the T-cell receptor gene rearrangement.

The HTLV-I integrated cell lines originated from human cord blood mononuclear cells were examined for the T-cell receptor beta chain gene rearrangement in conjunction with immunological phenotype analysis. Five of seven cell lines contained the rearranged T-cell receptor beta chain gene. Interestingly, most of the rearranged lines failed to express the T cell differentiation antigens, OKT 4 and 8, though their positive expression of Leu 1 antigen indicated the commitment to the T-cell lineage. On the other hand, two cell lines retained the germ-line configuration of the beta chain gene, while phenotypical examination revealed that the two cell lines have distinct T-cell antigens. Non-rearranged cell lines have proved to be nearly monoclonal from HTLV-I integration pattern and/or surface marker clonality. Thus, the relationship between the immunological phenotypes and the T-cell receptor gene rearrangement observed in the T-cell lineage is not strict and often dissociates. A possible involvement of HTLV-I infection on the dissociation between phenotype and genotype is discussed from the viewpoint of phenotypical modulation.

Antigens, Surface↗

PubMed2001

Conditioned medium from HeLa cells enhances motility of human monocyte-derived dendritic cells but abrogates their maturation and endocytic activity.

Progressive tumor proliferation may be associated with suppression of the immune response. Several different mechanisms can contribute to immune evasion. It is generally proposed that inhibition of dendritic cell functions would be a key mechanism by which tumors could escape immune surveillance. Therefore, the purpose of this study was to evaluate the capacity of HeLa cells conditioned medium (HeLa-CM) to modulate phenotypic and functional parameters of human peripheral blood monocyte-derived dendritic cells (DCs). Two types of reference DCs population were generated in vitro, the first cultured in the presence of IL-4 and GM-CSF which represented immature DCs (iDCs) and the second, representing mature DCs (mDCs), was raised from the iDCs by additional stimulation with a maturation cocktail - TNF-alpha, IL-1beta, IL-6, PGE2. In parallel, the iDCs were treated with HeLa-CM collected from the tumor cells. The analysis of DC populations demonstrated that the HeLa-CM prevented maturation of these cells and also impaired their capacity to uptake an antigen and stimulate proliferation of allogeneic T cells. In contrast, HeLa-CM modulated DCs exhibited a 3-fold increase mobility over iDCs. The latter functional capacity did not correlate with the levels of matrix metalloproteinase expression in the analysed cells. Altogether, our results provide evidence that HeLa cells produce soluble factors that might dramatically alter basic phenotypic and functional characteristics of DCs.

Cell Movement↗

PubMed2005

Oxidative stress produced with cell migration increases synthetic phenotype of vascular smooth muscle cells.

Phenotypic modulation of vascular smooth muscle cells (VSMC) and reactive oxygen species (ROS) is important in vascular pathogenesis. Understanding how these factors relate to cell migration can improve design of therapeutic interventions to control vascular disease. We compared the proliferation, protein content and migration of cultured aortic VSMC from wild type (WT) versus transgenic mice (Tgp22phox), in which overexpression of p22phox was targeted to VSMC. Also, we compared H2O2 generation and expression of specific phenotypic markers of non-migrating with migrating WT versus Tgp22phox VSMC in an in vitro wound scratch model. Enhanced H2O2 production in Tgp22phox versus WT VSMC (p < 0.005) significantly correlated with increased protein content, proliferation, and migration. VSMC migrating across the wound edge produced more H2O2 than non-migrating VSMC (p < 0.05). The expression of synthetic phenotypic markers, tropomyosin 4 and myosin heavy chain embryonic (SMemb), was enhanced significantly, while the expression of contractile marker, smooth muscle alpha-actin, was reduced significantly in migrating versus non-migrating cells, and also in Tgp22phox versus WT (p < 0.005) VSMC. These results are consistent with increased production of ROS accelerating the switch from the contractile to the synthetic phenotype, characterized by increases in proliferation, migration, and expression of TM4 and SMemb and decreased alpha-actin.

Animals↗

PubMedDate not supplied

Fibrosarcoma mimicking plasmacytoma or carcinoma: an ultrastructural study of 4 cases.

Because the fibroblast has a remarkable capability of phenotypic modulations, reflected in both morphologic and immunohistochemical (IHC) changes, ultrastructural studies are mandatory to identify the variants of fibroblasts. Myofibroblasts or histiofibroblasts are such examples, demonstrating chimeric ultrastructural features of fibroblastic cells in common with smooth muscle cells or with histiocytes, respectively. The presence of epithelioid fibroblastic cells sharing morphologic features with epithelial or plasma cells has not been yet characterized. The authors identified 4 cases of fibrosarcomas (FS) characterized by an unusual phenotype and associated with peculiar ultrastructural findings. The electron microscopic (EM) findings were correlated with the histologic appearance and immunoprofile. All tumors were located in the extremities, 3 in soft tissues and 1 in the bone. By light microscopy 2 cases were composed predominantly by round uniform cells with a striking plasmacytoid appearance. One case mimicked carcinoma, composed predominantly by epithelioid cells and scattered giant tumor cells. The fourth case showed a mixture of plasmacytoid-like and epithelioid cells. By IHC, tumor cells were positive for vimentin and in 2 cases also for epithelial membrane antigen. Kappa/lambda light chain and cytokeratins markers were negative. By EM all 4 tumors showed in addition to classic features of fibroblasts, unusual epithelial-type features, such as secretory granules of "neurosecretory-type" (3 cases), rudimentary cell junctions (3 cases), microvilli (2 cases), and lumen-like structures (1 case). One plasmacytoid-type tumor showed finely granular extracellular deposits. The study describe 4 examples of fibrosarcomas with unusual features at the ultrastructural level, which are associated microscopically with a peculiar phenotype, mimicking plasmacytoma or carcinoma. These findings broaden the spectrum of fibroblastic cell variants in neoplasia.

Adult↗

PubMed1998

Familial hypertrophic cardiomyopathy: a paradigm of the cardiac hypertrophic response to injury.

Hypertrophic cardiomyopathy (HCM) is an autosomal dominant disease caused by mutations in sarcomeric proteins. It is characterized by left ventricular hypertrophy in the absence of an increased external load, and myofibrillar disarray. While hypertrophy is a common cardiac response to injury, disarray is the pathological hallmark of HCM. A large number of mutations in genes coding for sarcomeric proteins, ie the beta-myosin heavy chain (beta-MyHC), cardiac troponin (cTn)T, cTnI, alpha-tropomyosin, myosin-binding protein C (MyBP-C), and essential and regulatory myosin light chains in patients with HCM have been identified. Genotype-phenotype correlation studies have shown that mutations carry prognostic significance. Unlike mutations in the beta-MyHC gene, the prognostic significance of which reflect their hypertrophic expressivity, cTnT mutations are associated with a mild degree of hypertrophy, but a high incidence of sudden cardiac death. Mutations in MyBP-C are associated with mild hypertrophy, and a benign prognosis. However, the genetic background in which the mutations occur, and possibly environmental factors also, modulate phenotypic expression of HCM. Functional studies of mutations causing HCM have shed significant light into the pathogenesis of HCM and have led to the hypothesis that mutant sarcomeric proteins function as 'poison peptides' exerting a dominant-negative effect on the function of the cardiac myocytes, followed by structural changes and a compensatory hypertrophy.

Animals↗

PubMed1999

Matrix metalloproteinase can facilitate the heparanase-induced promotion of phenotype change in vascular smooth muscle cells.

Previous studies from this laboratory have shown that degradation of heparan sulphate proteoglycan by both living macrophages and macrophage lysosomal heparanase induces phenotypic change of vascular smooth muscle cells (SMC) from a high volume fraction of myofilaments (V(v)myo) to a low V(v)myo [Campbell et al. Exp Cell Res 1992; 200: 156-167]. The aim of this study was to determine whether matrix metalloproteinase (MMP) activity is also involved in the induction of SMC phenotypic change by macrophages. A specific inhibitor of MMPs (BB94) was able to block macrophage-induced SMC phenotypic change and subsequent DNA synthesis in freshly dispersed SMC seeded in primary culture at confluent density. The inhibitor did not block these SMC changes when SMC were seeded at low density without macrophages nor did it block heparanase activity directly. We also determined whether heparanase and MMP activities are upregulated together in vivo. Artery homogenates were analysed in a heparanase enzyme assay and for MMPs using zymograms. Increased heparanase activity was observed 3-14 days following balloon catheter injury of rabbit carotid arteries, and returned to control levels 6 weeks after injury. Active MMP2 was induced with heparanase after injury. MMP9 induction was also apparent 6 h after injury. Immunohistology on sections of these arteries showed the presence of MMPI1, 2, 3 and 9 with these MMPs being strongly induced in the intima 7 days after balloon catheter injury. Both heparanase and MMP activities were also present in human end-stage complex lesions from coronary arteries, carotid endarterectomies and abdominal aortic aneurysms. Because MMPs and heparanase are expressed at the same time, it is possible that MMPs facilitate heparanase activity in promotion of phenotypic modulation of SMC in vivo during neointimal thickening following injury and in atherosclerotic lesions.

Actin Cytoskeleton↗

PubMed1991

[Arthritis from a biochemical aspect].

The dynamic processes of remodeling and cartilage destruction occurring in osteoarthritis are associated with an altered metabolism of the chondrocytes. Two mechanisms can be made responsible for chondrocyte activation: Stimulation by cytokines (mainly interleukin-1) and phenotypic modulation. Remodeling of osteoarthritic joint structures is associated with cell proliferation and neovascularization, while erosion of the articular cartilage is promoted by a variety of endopeptidases of chondrocytic origin. These aspects are briefly reviewed in the light of recent findings.

Cartilage, Articular↗

PubMed1996

Developmental pattern of expression and genomic organization of the calponin-h1 gene. A contractile smooth muscle cell marker.

Calponin-h1 is a 34-kDa myofibrillar thin filament, actin-binding protein that is expressed exclusively in smooth muscle cells (SMCs) in adult animals. To examine the molecular mechanisms that regulate SMC-specific gene expression, we have examined the temporal, spatial, and cell cycle-regulated patterns of expression of calponin-h1 gene expression and isolated and structurally characterized the murine calponin-h1 gene. Calponin-h1 mRNA is expressed exclusively in SMC-containing tissues in adult animals. During murine embryonic development, calponin-h1 gene expression is (i) detectable in E9.5 embryos in the dorsal aorta, cardiac outflow tract, and tubular heart, (ii) sequentially up-regulated in SMC-containing tissues, and (iii) down-regulated to non-detectable levels in the heart during late fetal development. In addition, the gene is expressed in resting rat aortic SMCs, but its expression is rapidly down-regulated when growth-arrested cells reenter phase G1 of the cell cycle and proliferate. Calponin-h1 is encoded by a 10.7-kilobase single copy gene composed of seven exons, which is part of a multigene family. Transient transfection analyses demonstrated that 1.5 kilobases of calponin-h1 5'-flanking sequence is sufficient to program high level transcription of a luciferase reporter gene in cultured primary rat aortic SMCs and the smooth muscle cell line, A7r5. Taken together, these data suggest that the calponin-h1 gene will serve as an excellent model system with which to examine the molecular mechanisms that regulate SMC lineage specification, differentiation, and phenotypic modulation.

Amino Acid Sequence↗