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Results for “Phenotypic modulation”

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At least 199 records · Page 11Linked to original sources
PubMed1995

Phenotypic modulation of gonococcal lipooligosaccharide in acidic and alkaline culture.

Neisseria gonorrhoeae infects a diverse array of niches in its human host, which expose the organism to dramatic variations in pH. We examined growth and lipooligosaccharide expression of two gonococcal strains in liquid and solid cultures under acidic, neutral, and alkaline conditions. Growth rates in broth were similar under the three conditions, and the pH remained fairly constant throughout the growth cycle. Altered lipooligosaccharide expression at the different pHs was noted in both plate- and broth-grown organisms.

Bacterial Proteins↗
PubMed1999

[Development of new anti-atherosclerotic drugs based on the phenotypic modulation of vascular smooth muscle cells].

We have established a novel smooth muscle cell line (SVS) which retains the expression of specific markers for smooth muscle cells, such as smooth muscle myosin-1, calponin and SM22 alpha, from temperature-sensitive SV40 large T-antigen transgenic mice. SVS cells showed temperature-dependent growth and the expression of smooth muscle markers, showing that the differentiation stage can be controlled in this cell line by culture temperature. We have constructed luciferase-reporter cell lines for calponin and SM22 alpha genes by using SVS cells. We detected some compounds including ascorbic acid, which stimulated the expression of smooth muscle markers by the reporter assay. Ascorbic acid and its long lasting derivatives stimulated the expression of markers continuously. Moreover, ascorbic acid activated the expression of markers in synthetic SMCs seen in the intima of a rat balloon injury model. Thus, this reporter system should be useful for discovery of new antiatherosclerotic drugs.

Animals↗
PubMed2002

Phenotypic modulation of fibroblastic cells in the mucous layer of the human uterine cervix at term.

The uterine cervix is a dynamic structure with a high capacity to adapt to different, even opposing, roles during the sequence of physiological events of gestation (for example, acting as a barrier to retain the fetus during pregnancy and dilating to allow delivery at term). Histoarchitectural changes of the uterine cervix allow its successful adaptation. The aim of this study was to investigate whether fibroblastic cell plasticity, described in the lamina propria of the rat uterine cervix at term, could be observed in women too. Biopsy specimens of non-pregnant and intrapartum human cervices were studied under the transmission electron microscope, and cytoskeletal differentiation markers were identified by immunohistochemistry under the light microscope. Desmin-positive cells were present in the mucous layer of the cervix during labour. These cells displayed cytoplasmic processes (typical of myofibroblasts) that also stained positively for vimentin. The main ultrastructural features for defining the myofibroblast under the electron microscope were also observed in these cells. However, cervices of non-pregnant women contained resident fibroblasts at the same location. Examination of the differentiation repertoire of fibroblastic cells in the mucous layer of the uterine cervix resulted in the characterization of myofibroblasts at term. The implications of the plasticity of fibroblastic-myofibroblastic cells in the physiological changes displayed in the uterine cervix during pregnancy, labour and postpartum involution require further investigation.

Biomarkers↗
PubMed1983

Modulation of phenotype in cultures of human milk epithelial cells and its relation to the expression of a membrane antigen.

Primary cultures of human milk epithelial cells, labelled with HMFG-1, a monoclonal antibody that recognises a differentiation antigen on the membranes of breast epithelia, were separated from unlabelled cells in a fluorescence-activated cell sorter (FACS). Cells not expressing the HMFG-1 antigen have a greater in vitro growth potential than the positive ones, and give rise to cultures containing both HMFG-1 antigen positive and negative cells. The cultures derived from negative cells usually contain colonies with 'open' cuboidal cells and these do not express the HMFG-1 antigen. However, when they differentiate into other phenotypes such as the 'closed' cuboidal cell type, expression of the differentiation antigen becomes evident and the cultures then show a reduced growth potential. When milk cells are subcultured several times, a new cell type emerges which does not express the HMFG-1 antigen or the intermediate filaments typical of epithelial cells but instead express high levels of fibronectin which is found in an extracellular matrix. Whether these cells emerge by selection of an existing phenotype or by phenotypic modulation is discussed.

Antibodies, Monoclonal↗
PubMed2000

Regulation of human COL2A1 gene expression in chondrocytes. Identification of C-Krox-responsive elements and modulation by phenotype alteration.

To identify control motifs involved in human type II collagen gene transcription in both differentiated and dedifferentiated rabbit articular chondrocytes, transient transfection experiments were performed. A 715-base pair (bp) region of the first intron (+2127/+2842), including a 153-bp sequence so far uncharacterized (+2689/+2842), was found to mediate enhancer activity. In dedifferentiated chondrocytes, this enhancer activity was shown to be less effective than in primary cultures but still present. We then demonstrated that a zinc finger protein, C-Krox, activates COL2A1 gene transcription in differentiated chondrocytes through the enhancer region, whereas in subcultured cells, it inhibited the gene activity via a 266-bp promoter. Multicopies of the C-Krox binding site were found to mediate transactivation in both primary cultures and passaged cells, whereas C-Krox overexpression inhibited transcription in dedifferentiated chondrocytes. Additionally, we showed that C-Krox binds to several cis sequences that mediate its transcriptional effects. During chondrocyte dedifferentiation, the protein levels and binding activity of C-Krox were reduced, whereas those of NF-kappaB were increased. This was not associated with variations of mRNA levels, suggesting that post-transcriptional regulatory mechanisms could be involved in C-Krox expression. These results suggest that C-Krox plays a major role in type II collagen expression and the chondrocyte phenotype modulation.

Animals↗
PubMed1997

Transforming growth factor-beta 1 modulates myofibroblastic phenotype of rat palatal fibroblasts in vitro.

The effects of transforming growth factor-beta 1 (TGF-beta 1) on normal rat palatal fibroblasts in vitro were investigated in the present study in order to unravel the precise mechanisms by which the phenotypic modulation of fibroblasts occurs during the scar formation process. TGF-beta 1 dramatically changed the morphology of normal palatal fibroblasts from polygonal into an elongated shape, which was very similar to that of fibroblasts derived from experimental immature scar tissue in rat palatal mucosa. This morphological transition was concomitant with an increase in the expression of alpha-smooth muscle (alpha-SM) actin protein, a marker for myofibroblasts, when determined by immunocytochemistry. An immunoblot study also revealed that alpha-SM actin expression in palatal fibroblasts became evident after 24 h of TGF-beta 1 treatment and increased time-dependently up to 72 h. Northern blot analysis showed that TGF-beta 1 stimulated endogenous TGF-beta 1 mRNA expression in palatal fibroblasts within 24 h. Neither epidermal growth factor nor basic fibroblast growth factor had any effect on either alpha-SM actin expression or TGF-beta 1 mRNA expression. Pretreatment of palatal fibroblasts with TGF-beta 1 significantly increased the contractile capacity in a three-dimensional collagen gel culture, even when the culture medium was deprived of TGF-beta 1 for 72 h of the experimental period. Moreover, the contractility of scar fibroblasts, which highly expressed alpha-SM actin protein and TGF-beta 1 mRNA, was significantly lowered by a neutralizing antibody to TGF-beta 1. These data strongly suggest that TGF-beta 1 is a potential inducer of phenotypic expression of myofibroblasts in palatal fibroblasts and that auto-induction of TGF-beta 1 mRNA expression may play an important role in the scar formation process in palatal mucosa.

Actins↗
PubMed2026

Generation and validation of a Myh11Dre-Spp1Cre intersectional mouse model for lineage tracing of disease-associated smooth muscle cell states.

BACKGROUND: Phenotypic modulation of vascular smooth muscle cells (VSMCs) is a hallmark of vascular remodeling and cardiovascular disease. Recent lineage-tracing and single-cell transcriptomic studies have identified secreted phosphoprotein 1 (SPP1) as a prominent marker associated with disease-associated VSMC states, particularly those linked to fibrotic remodeling and vascular calcification. However, the cellular origins and fate of SPP1-associated VSMC populations remain incompletely understood. METHODS AND RESULTS: We generated a novel Spp1-rSTOPr-Cre (Spp1Cre) knock-in mouse line in which Cre recombinase is expressed from the endogenous Spp1 locus following Dre-mediated excision of a rox-flanked transcriptional STOP cassette. Correct targeting of the knock-in allele was validated by internal, 5' junction, 3' junction, and long-range PCR analyses, as well as Sanger sequencing. To establish an intersectional lineage-tracing strategy, Spp1Cre mice were crossed with Myh11DreERT2 and Rosa26-RSR-LSL-tdTomato-LSL-eGFP reporter mice, enabling permanent labeling of VSMC-derived populations following activation of the endogenous Spp1 locus. Under physiological conditions, eGFP-positive cells were detected at low frequency within the vascular wall and were predominantly negative for the contractile markers ACTA2 and MYH11. As a proof-of-principle application, eGFP-positive cells markedly expanded within atherosclerotic lesions induced by AAV-PCSK9D377Y and high-fat diet feeding. These lineage-traced cells remained largely ACTA2- and MYH11-negative, consistent with a modulated phenotype. Notably, only a minority of eGFP-positive cells expressed SPP1 or fibronectin at the time of analysis, demonstrating the utility of permanent lineage tracing for tracking cells with a history of endogenous Spp1 activation during vascular remodeling. CONCLUSION: We report the generation and validation of a novel Myh11Dre-Spp1Cre intersectional mouse model for lineage tracing of VSMC-derived populations that have activated the endogenous Spp1 locus. This genetic resource provides a valuable platform for investigating the origin, fate, and phenotypic evolution of Spp1-associated VSMC populations during vascular remodeling and cardiovascular disease.

Animals↗
PubMedDate not supplied

[The modulation of the phenotype of the human hepatoblastoma cell line HepG2 under the action of dimethyl sulfoxide].

Phenotype modulation of the human hepatoblastoma cells HepG2 treated with dimethyl sulfoxide (DMSO) was studied using indirect immunoperoxidase method with monoclonal antibodies against antigens with characteristic localization in the adult liver: cytokeratin 18, membrane antigen AGS5 and embryo-specific alpha-fetoprotein (AFP). Untreated HepG2 cells were found to contain all these antigens. However, their localization was different from that in the adult human liver. Instead of submembrane layer characteristic of liver parenchyma cells in situ, cytokeratin in HepG2 cells formed a cytoplasmic network and bundles. Membrane antigen AGC5 in HepG2 cells was fond only in the cytoplasm. Most HepG2 cells contained AFP which is absent from the adult liver cells. Under the effect of DMSO the "adult" type of cytokeratin 18 and AGS5 localization was re-established only in cells organized in dense cell layers, while in single cells or poorly compacted cell islets it remained unchanged. Treatment of HepG2 cells with DMSO resulted in a drastic decrease in the rate of AFP secretion, as well as in AFP-specific staining of either single cells or cell islets and layers. We suggest that the effect of DMSO on cell differentiation is mediated by different mechanisms. One of them can be associated with cell-to-cell interactions, while another with the direct interaction between DMSO and individual cells.

Antibodies, Monoclonal↗
PubMed1997

Proliferation of smooth muscle cells in acute allograft vascular rejection.

OBJECTIVES: To determine whether immune injury during acute cardiac rejection induces phenotypic modulation of arterial smooth muscle cells and lesion formation, we studied the expression of embryonic myosin heavy-chain isoform and degrees of intimal proliferation in aortas and coronary arteries of allografted rabbit hearts. Modulation of phenotype in arterial smooth muscle cells during acute vascular injury is a widely reported phenomenon, and proliferation and migration of medial smooth muscle cells contribute to development of intimal hyperplasia of arteries in response to immune injury. METHODS: Rabbit hearts were heterotopically transplanted to the neck without immunosuppression. Hearts were harvested at 2, 5, 7, and 10 days after transplantation. Proliferation of smooth muscle cells was assessed by bromodeoxyuridine labeling. Staining for immunohistochemical indicators was done with use of monoclonal antibodies that recognize T lymphocytes and all types of smooth muscle cells (SM1), adult type of smooth muscle cells (SM2), and embryonic myosin heavy-chain isoform. Intimal thickening and luminal narrowing were assessed with a computer-assisted video image analysis system. RESULTS: Intimal thickening and luminal narrowing in aortas and coronary arteries gradually increased in a time-dependent manner. The neointima thus formed consisted of proliferating smooth muscle cells positive for both SM1 and embryonic myosin heavy-chain isoform and massive T lymphocyte accumulation. Intimal proliferation was more prominent in aortas and large epicardial coronary arteries than in the intramyocardial small coronary arteries. CONCLUSIONS: These findings suggest that allogeneic immune injury facilitates phenotypic modulation of smooth muscle cells, which may contribute to subsequent transplantation-associated atherosclerosis.

Animals↗
PubMed2003

Krüppel-like factor 4 (KLF4/GKLF) is a target of bone morphogenetic proteins and transforming growth factor beta 1 in the regulation of vascular smooth muscle cell phenotype.

Vascular smooth muscle cell (VSMC) differentiation and phenotypic modulation is characterized by changes in mRNA expression for smooth muscle (SM) marker contractile proteins such as alpha-SM actin and SM22 alpha. Transforming growth factor beta1 (TGF-beta 1) is a potent VSMC differentiation factor; however, it is not known if other TGF-beta-superfamily members, in particular the bone morphogenetic proteins (BMPs), modulate VSMC phenotype. Here we demonstrate that a large subset of TGF-beta-superfamily members and their type I receptors are differentially co-expressed as VSMC phenotype changes during fetal/neonatal development and that BMP2, -4, and -6 reciprocally regulate SM-marker mRNA and protein expression in vitro. BMP2 and BMP6 decrease expression of the SM markers alpha-SM actin, SM22alpha, and calponin in rat VSMCs, whereas BMP4 increases their expression. The effects of BMP-2, -4, and -6 on SM marker gene transcription are mediated through a consensus TGF-beta-controlling element, the TCE, which is common to regulatory regions of SM-marker genes. Moreover, co-treatment experiments revealed that BMP-2, -4, and -6 each inhibit TGF-beta 1-modulated increases in SM22alpha reporter gene activity. Regardless of whether they positively or negatively regulate SM marker expression, TGF-beta 1 and BMP-2, -4, and -6 all induced binding of the Krüppel-like transcription factor, GKLF/KLF4, to the TGF-beta control element. Induction of KLF4 was confirmed by immunocytochemistry and Western blotting, which revealed that a lower molecular weight KLF4 protein is induced after treatment with TGF-beta-superfamily members. Taken together, our results demonstrate that multiple members of the TGF-beta superfamily act in concert to modulate VSMC phenotype.

Actins↗
PubMed1987

Modulation of the metastatic phenotype by 13-cis-retinoic acid.

KLN 205 murine squamous carcinoma cells were grown in medium supplemented with the retinoid 13-cis-retinoic acid (RA) to study the relationship between RA-induced cell surface changes and alterations of the metastatic phenotype. Modulation of the cell surface glycoconjugate expression was measured by flow cytometric analysis of the RA-treated tumor cells stained with fluoresceinated lectins. RA treatment (5 X 10(-6) and 5 X 10(-7) M) altered the glycoconjugate expression of KLN 205 cells in a selective, dose-dependent fashion. Tumor cells grown in RA-supplemented medium for more than 4 days demonstrated greatly increased binding of fluoresceinated Griffonia simplicifolia I lectin, peanut lectin, wheat-germ lectin, concanavalin A, and soybean lectin (P less than .001), but the increased binding of Ulex europaeus lectin was of a much smaller magnitude (P = .02). After 15 days of growth in these noncytotoxic or cytostatic concentrations of RA, malignant KLN 205 cells had a greatly decreased proclivity to metastasize, as measured by the lung colony assay (P = .0003). The RA-induced cell surface glycoconjugate changes preceded the decrease in experimental metastatic potential. Since enzymatic (neuraminidase) alteration of the tumor cell surface to produce glycoconjugate expression similar to that seen in RA-treated cells also reduced the ability of the KLN 205 cells to form lung colonies (P = .0022), it is suggested that RA-induced alteration of the cell surface carbohydrate antigens is related to the decreased experimental metastatic potential seen in tumor cells treated with RA.

Animals↗
PubMed1996

Angiotensin II and calcium blockers prevent glomerular phenotypic changes in remnant kidney model.

Recent studies on various models of glomerular diseases indicate that glomerular injury is associated with the phenotypic modulation of glomerular cells. However, the effect of renoprotective agents on glomerular phenotype remains to be determined. This study examined the effects of angiotensin II Type 1 (AT1) receptor antagonists and calcium antagonists on glomerular phenotypic changes in rats with subtotal renal ablation. Rats were subjected to 5/6 nephrectomy and were given oral TCV-116, a selective AT1 receptor antagonist (1 mg/kg), manidipine, a dihydropyridine calcium antagonist (3 mg/kg), or vehicle for 8 wk. Glomerular phenotypic modulation was determined by the staining of alpha-smooth muscle actin and desmin in glomerular cells with an immunohistochemical technique. At the start of drug treatment, alpha-smooth muscle actin and desmin were already significantly expressed in the glomerular cells of 5/6-nephrectomized rats, in contrast to a negligible glomerular expression of these proteins in sham-operated rats. Treatment of 5/6-nephrectomized rats with TCV-116 or manidipine significantly decreased glomerular expression of alpha-smooth muscle actin and desmin, thereby indicating that these drugs prevented glomerular phenotypic changes in 5/6-nephrectomized rats. Furthermore, their inhibitory effects on glomerular phenotypic modulation were associated with the prevention of glomerular cell proliferation, hypertrophy, and sclerosis. Therefore, this study provides the first evidence that the renoprotection is linked to the prevention of glomerular phenotypic modulation and supports the idea that this phenotypic modulation may serve as an important cellular marker of glomerular injury.

Actins↗
PubMed1993

Type I collagen promotes modulation of cultured rabbit arterial smooth muscle cells from a contractile to a synthetic phenotype.

The phenotypic transition of smooth muscle cells (SMC) from a contractile to a synthetic state appears to be an early event in the pathogenesis of atherosclerosis. We examined the effects of extracellular matrix components on the phenotypic modulation of rabbit arterial SMC in primary culture by flow cytometry. The results demonstrate that freshly isolated SMC attached, spread, and started to proliferate on type I collagen as well as on fibronectin. Moreover, type I collagen was as efficient as fibronectin in promoting the transition of the cells into the synthetic phenotype without exogenous mitogens. However, unlike on fibronectin, the synthetic peptide GRGDSP (Gly-Arg-Gly-Asp-Ser-Pro) and the peptide KDGEA (Lys-Asp-Gly-Glu-Ala), which contains the recognition sequence for alpha 2 beta 1 integrin in type I collagen, interfered little with the attachment, spreading, and phenotypic modulation of the cells on type I collagen. On the other hand, the phenotypic modulation of the cells was counteracted by the anti-beta 1 integrin antibody. These findings indicate that type I collagen promotes the phenotypic transition of the rabbit arterial SMC by interacting with a cell surface receptor (beta 1 integrin family) for a cell-binding sequence without RGD and DGEA. In contrast, elastin, a major constituent of the media, suppressed the cell attachment and spreading and maintained the cells in the contractile phenotype as laminin. These results suggest diverse roles of type I collagen and elastin as well as of fibronectin and laminin in the control of the differentiated properties of arterial SMC.

Amino Acid Sequence↗
PubMed2001

Short chain fatty acids differentially modulate cellular phenotype and c-myc protein levels in primary human nonmalignant and malignant colonocytes.

Short chain fatty acids may protect colonic mucosa against neoplastic transformation by modulating colonocyte phenotype, DNA synthesis, and c-myc levels. To test this hypothesis, nonmalignant and malignant human colonocytes were isolated from surgical specimens and treated with 10 mM acetate, propionate, or butyrate. Markers of cellular phenotype, DNA synthesis, and c-myc protein levels were assayed by alkaline phosphatase and dipeptidyl dipeptidase IV activities, [3H]thymidine labeling, and western blotting, respectively. Butyrate, in particular, exerted discordant effects on alkaline phosphatase (P < 0.05), and c-myc levels (P < 0.05, N > or = 6) in nonmalignant and malignant human colonocytes. DPDD was unaffected by any of the short chain fatty acids tested. [3H]Thymidine labeling was differentially stimulated by short chain fatty acids in both cell types and greater DNA synthesis rates were observed in malignant colonocytes (P < 0.005, N = 16). These data suggest that in vitro, butyrate, in particular, may differentially modulate phenotype, DNA synthesis, and c-myc in nonmalignant and malignant human colonocytes.

Aged↗
PubMed2006

Mutation in TRMU related to transfer RNA modification modulates the phenotypic expression of the deafness-associated mitochondrial 12S ribosomal RNA mutations.

The human mitochondrial 12S ribosomal RNA (rRNA) A1555G mutation has been associated with aminoglycoside-induced and nonsyndromic deafness in many families worldwide. Our previous investigation revealed that the A1555G mutation is a primary factor underlying the development of deafness but is not sufficient to produce a deafness phenotype. However, it has been proposed that nuclear-modifier genes modulate the phenotypic manifestation of the A1555G mutation. Here, we identified the nuclear-modifier gene TRMU, which encodes a highly conserved mitochondrial protein related to transfer RNA (tRNA) modification. Genotyping analysis of TRMU in 613 subjects from 1 Arab-Israeli kindred, 210 European (Italian pedigrees and Spanish pedigrees) families, and 31 Chinese pedigrees carrying the A1555G or the C1494T mutation revealed a missense mutation (G28T) altering an invariant amino acid residue (A10S) in the evolutionarily conserved N-terminal region of the TRMU protein. Interestingly, all 18 Arab-Israeli/Italian-Spanish matrilineal relatives carrying both the TRMU A10S and 12S rRNA A1555G mutations exhibited prelingual profound deafness. Functional analysis showed that this mutation did not affect importation of TRMU precursors into mitochondria. However, the homozygous A10S mutation leads to a marked failure in mitochondrial tRNA metabolisms, specifically reducing the steady-state levels of mitochondrial tRNA. As a consequence, these defects contribute to the impairment of mitochondrial-protein synthesis. Resultant biochemical defects aggravate the mitochondrial dysfunction associated with the A1555G mutation, exceeding the threshold for expressing the deafness phenotype. These findings indicate that the mutated TRMU, acting as a modifier factor, modulates the phenotypic manifestation of the deafness-associated 12S rRNA mutations.

Amino Acid Sequence↗
PubMed1996

Scleroderma fibroblast phenotype is modulated by endothelial cell co-culture.

OBJECTIVE: We established a co-culture system to investigate endothelial cell-fibroblast interaction in scleroderma (systemic sclerosis, SSc). Such a system allows reciprocal interaction between these cells. The pattern of phenotypic modulation for normal and SSc fibroblasts in co-culture was compared. METHODS: A virally transformed human umbilical vein endothelial cell (HUVEC) derived cell line (1E-7) was cultured on nitrocellulose membrane inserts above dermal fibroblast monolayers. The effect of co-culture on fibroblast number, [3H]-thymidine ([3H]-TdR) incorporation, and collagen (type I) production were compared for 10 SSc and 5 control cell lines. Co-culture with the epithelial lines A549 and A431, and nontransformed HUVEC, was also investigated. RESULTS: We observed a statistically significant increase in cell number and a reduction in collagen production for SSc, but not control, fibroblasts co-cultured with endothelial cells. This co-culture also promoted [3H]-TdR incorporation in both SSc and control fibroblasts. While epithelial cell lines did not influence fibroblast cell number, collagen production by SSc fibroblasts was diminished by A549. CONCLUSIONS: Endothelial cell derived soluble factors modulated fibroblast properties in co-culture, and the different response of SSc compared with normal fibroblasts provides further evidence for a link between endothelial and fibroblast dysfunction in this disease. However, similar effects on SSc fibroblast collagen production were also observed for some epithelial cells, suggesting that modulation of fibroblast properties is not restricted to cells of endothelial origin.

Adult↗
PubMed1985

Adult human arterial smooth muscle cells in primary culture. Modulation from contractile to synthetic phenotype.

Smooth muscle cells were isolated enzymatically from adult human arteries, grown in primary culture in medium containing 10% whole blood serum, and studied by transmission electron microscopy and [3H]thymidine autoradiography. In the intact arterial wall and directly after isolation, each smooth muscle cell had a nucleus with a wide peripheral zone of condensed chromatin and a cytoplasm dominated by myofilament bundles with associated dense bodies. After 1-2 days of culture, the cells had attached to the substrate and started to spread out. At the same time, a characteristic fine-structural modification took place. It included nuclear enlargement, dispersion of the chromatin and formation of large nucleoli. Moreover, myofilament bundles disappeared and an extensive rough endoplasmic reticulum and a large Golgi complex were organized in the cytoplasm. This morphological transformation of the cells was completed in 3-4 days. It was accompanied by initiation of DNA replication and mitosis. The observations demonstrate that adult human arterial smooth muscle cells, when cultivated in vitro, pass through a phenotypic modulation of the same type as arterial smooth muscle cells from experimental animals. This modulation gives the cells morphological and functional properties resembling those of the modified smooth muscle cells found in fibroproliferative lesions of atherosclerosis. Further studies of the regulation of smooth muscle phenotype and growth may provide important clues for a better understanding of the pathogenesis of atherosclerosis.

Adult↗