Phenotypic Modulation of Smooth Muscle Cells after Arterial Injury Is Associated with Changes in the Distribution of Laminin and Fibronectin

1997 ◽  
Vol 45 (6) ◽  
pp. 837-846 ◽  
Author(s):  
Johan Thyberg ◽  
Karin Blomgren ◽  
Joy Roy ◽  
Phan Kiet Tran ◽  
Ulf Hedin
Keyword(s):  
Smooth Muscle ◽  
Basement Membrane ◽  
Smooth Muscle Cells ◽  
Actin Filaments ◽  
Cell Structure ◽  
Muscle Cells ◽  
Arterial Injury ◽  
Internal Elastic Lamina ◽  
Contractile Phenotype

Earlier in vitro studies suggest opposing roles of laminin and fibronectin in regulation of differentiated properties of vascular smooth muscle cells. To find out if this may also be the case in vivo, we used immunoelectron microscopy to study the distribution of these proteins during formation of intimal thickening after arterial injury. In parallel, cell structure and content of smooth muscle α-actin was analyzed. The results indicate that the cells in the normal media are in a contractile phenotype with abundant α-actin filaments and an incomplete basement membrane. Within 1 week after endothelial denudation, most cells in the innermost layer of the media convert into a synthetic phenotype, as judged by loss of actin filaments, construction of a large secretory apparatus, and destruction of the basement membrane. Some of these cells migrate through fenestrae in the internal elastic lamina and invade a fibronectin-rich network deposited on its luminal surface. Within another few weeks a thick neointima forms, newly produced matrix components replace the strands of fibronectin, and a basement membrane reappears. Simultaneously, the cells resume a contractile phenotype, recognized by disappearance of secretory organelles and restoration of α-actin filaments. These findings support the notion that laminin and other basement membrane components promote the expression of a differentiated smooth muscle phenotype, whereas fibronectin stimulates the cells to adopt a proliferative and secretory phenotype.

scholarly journals The effect of human growth hormone on the carbohydrate units in arterial basement membrane-like material

2000 ◽  
pp. 631-635 ◽  
Author(s):  
T Ledet ◽  
L Heickendorff
Keyword(s):  
Growth Hormone ◽  
Smooth Muscle ◽  
Basement Membrane ◽  
Smooth Muscle Cells ◽  
Human Growth Hormone ◽  
Human Growth ◽  
Muscle Cells ◽  
Carbohydrate Composition ◽  
Large Vessel Disease

OBJECTIVE: The present study focuses on the pathogenesis of the large vessel disease in diabetes. The arterial wall from diabetic individuals displays characteristic alterations of the extracellular matrix. Other observations show that the metabolism is changed with increased levels of growth hormone in diabetes. DESIGN: The effects of growth hormone on the carbohydrate composition in the basement membrane around the arterial smooth muscle cells were investigated. METHODS: Basement membrane material was obtained from cultures of smooth muscle cells by sonication and differential centrifugation after labeling with either [(3)H]glucose or [(3)H]glucosamine. The proportions of galactose, glucose, mannose, xylose, fucose and glucosamine were evaluated after addition of 45.45pmol/l human growth hormone. Also, the proportion of glycopeptides generated from the basement membrane was analyzed after fractionation on a combination of a Concanavalin A and a Pea Sepharose column. RESULTS: The proportion of galactose and glucose was changed, and the incorporation of [(3)H]glucosamine was reduced. The proportion of glycopeptides containing high mannose moities was increased as well as that of triantinary glycopeptides with internal fucose residues. CONCLUSION: The current in vitro data indicates that growth hormone may change the carbohydrate composition of the arterial basement membrane.

scholarly journals A novel mechanism of Euonymine inhibits in-stent restenosis through enhancing contractile phenotype of VSMCs by targeting AKT1 and p38MAPK

2021 ◽  
Author(s):  
Li Zhang ◽  
Yi Ting Tao ◽  
Qin Hu ◽  
Ren Hua Yang ◽  
Jia Jia ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Contractile Phenotype ◽  
Stent Restenosis ◽  
Drug Eluting ◽  
In Stent Restenosis

This study aimed to examine the inhibitory effects of Euonymine on in-stent restenosis (ISR) after percutaneous coronary intervention (PCI) and oxidized low-density lipoprotein (ox-LDL)-induced proliferation, migration, and pro-apoptotic of vascular smooth muscle cells (VSMCs) in vitro, and its potential mechanisms. Euonymine is a monomer component extracted from Tripterygium hypoglaucum (Levl) Hutch. Using in vitro models of rabbit carotid balloon injury and porcine atherosclerotic coronary implantation, we confirmed that Euonymine inhibited ISR after PCI. Furthermore, Euonymine inhibited VSMC phenotypic transformation by targeting AKT1 to regulate the PTEN/AKT1/m TOR signaling pathway, with exertion of anti-proliferative, anti-migratory, and pro-apoptotic effects on ox-LDL-induced cell injury model. Additionally, the study demonstrated that Euonymine induced apoptosis of VSMCs via the p38MAPK-related mitochondria-dependent apoptotic pathway. Collectively, these findings indicated that Euonymine drug-eluting stents inhibited ISR after PCI by targeting AKT1 and p38MAPK to enhance the contractile phenotype of VSMCs to prevent intimal hyperplasia development. This provides insights into a potential therapeutic strategy involving the beneficial effect of Euonymine drug-eluting stent on ISR. Keywords: Euonymine; Neointimal hyperplasia; Vascular smooth muscle cells, PTEN/AKT1/mTOR;p38MAPK; Proliferation; Migration; Apoptosis.

scholarly journals Roles of vascular endothelial and smooth muscle cells in the vasculoprotective effect of insulin in a mouse model of restenosis

2021 ◽  
Vol 18 (3) ◽  
pp. 147916412110273
Author(s):  
Yusaku Mori ◽  
Marel Gonzalez Medina ◽  
Zhiwei Liu ◽  
June Guo ◽  
Luke S Dingwell ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Insulin Treatment ◽  
Muscle Cells ◽  
Arterial Injury ◽  
Vascular Endothelial ◽  
Muscle Myosin

Background: Insulin exerts vasculoprotective effects on endothelial cells (ECs) and growth-promoting effects on vascular smooth muscle cells (SMCs) in vitro, and suppresses neointimal growth in vivo. Here we determined the role of ECs and SMCs in the effect of insulin on neointimal growth. Methods: Mice with transgene CreERT2 under the control of EC-specific Tie2 (Tie2-Cre) or SMC-specific smooth muscle myosin heavy chain promoter/enhancer (SMMHC-Cre) or littermate controls were crossbred with mice carrying a loxP-flanked insulin receptor (IR) gene. After CreERT2-loxP-mediated recombination was induced by tamoxifen injection, mice received insulin pellet or sham (control) implantation, and underwent femoral artery wire injury. Femoral arteries were collected for morphological analysis 28 days after wire injury. Results: Tamoxifen-treated Tie2-Cre+ mice showed lower IR expression in ECs, but not in SMCs, than Tie2-Cre− mice. Insulin treatment reduced neointimal area after arterial injury in Tie2-Cre− mice, but had no effect in Tie2-Cre+ mice. Tamoxifen-treated SMMHC-Cre+ mice showed lower IR expression in SMCs, but not in ECs, than SMMHC-Cre− mice. Insulin treatment reduced neointimal area in SMMHC-Cre− mice, whereas unexpectedly, it failed to inhibit neointima formation in SMMHC-Cre+ mice. Conclusion: Insulin action in both ECs and SMCs is required for the “anti-restenotic” effect of insulin in vivo.

Inducible PDGF A-chain transcription in smooth muscle cells is mediated by Egr-1 displacement of Sp1 and Sp3

1997 ◽  
Vol 273 (3) ◽  
pp. H1415-H1426 ◽  
Author(s):  
E. S. Silverman ◽  
L. M. Khachigian ◽  
V. Lindner ◽  
A. J. Williams ◽  
T. Collins
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Arterial Injury ◽  
In Vivo Model ◽  
Binding Assays ◽  
Base Pairs ◽  
A Chain

Platelet-derived growth factor (PDGF) A-chain is expressed by vascular smooth muscle cells (SMC) in a variety of pathological settings. Phorbol 12-myristate 13-acetate (PMA) increases A-chain transcription and was used as a model agonist. Transient transfection analysis identified a region in the promoter that is required for inducibility, located between base pairs -71 and -55 from the transcription start site. This region contains overlapping recognition elements for members of the Sp and Egr families. Egr-1 transcript and protein increased after PMA treatment, whereas Sp1 and Sp3 levels remain unchanged. Egr-1 expression and PDGF A-chain promoter activity also increased in cells exposed to PDGF or mechanical injury. In vitro binding assays demonstrated that Egr-1, Sp1, and Sp3 can bind to this promoter region and that increasing Egr-1 can displace both Sp1 and Sp3. In an in vivo model of arterial injury, Egr-1 expression was induced concurrently with the expression of PDGF-A in SMC. Displacement of Sp1 and Sp3 by Egr-1 is correlated with inducible PDGF A-chain expression in the vessel wall.

Epicardial Cells of Human Adults Can Undergo an Epithelial-to-Mesenchymal Transition and Obtain Characteristics of Smooth Muscle Cells In Vitro

Stem Cells ◽  
2007 ◽  
Vol 25 (2) ◽  
pp. 271-278 ◽  
Author(s):  
John van Tuyn ◽  
Douwe E. Atsma ◽  
Elizabeth M. Winter ◽  
Ietje van der Velde-van Dijke ◽  
Daniel A. Pijnappels ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Muscle Cells ◽  
Mesenchymal Transition ◽  
Epicardial Cells ◽  
Human Adults

Characterization and confocal imaging of calponin in gastrointestinal smooth muscle

1993 ◽  
Vol 265 (5) ◽  
pp. C1371-C1378 ◽  
Author(s):  
M. P. Walsh ◽  
J. D. Carmichael ◽  
G. J. Kargacin
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase ◽  
Smooth Muscle Cells ◽  
Thin Filament ◽  
Muscle Cells ◽  
Biochemical Properties ◽  
Confocal Imaging ◽  
Isolated Cells ◽  
Independent Manner

Calponin isolated from chicken gizzard smooth muscle binds in vitro to actin in a Ca(2+)-independent manner and thereby inhibits the actin-activated Mg(2+)-adenosinetriphosphatase of smooth muscle myosin. This inhibition is relieved when calponin is phosphorylated by protein kinase C or Ca2+/calmodulin-dependent protein kinase II, suggesting that calponin is involved in thin filament-associated regulation of smooth muscle contraction. To further examine this possibility, calponin was isolated from toad stomach smooth muscle, characterized biochemically, and localized in intact isolated cells. Toad stomach calponin had the same basic biochemical properties as calponin from other sources. Confocal immunofluorescence microscopy revealed that calponin in intact smooth muscle cells was localized to long filamentous structures that were colabeled by antibodies to actin or tropomyosin. Preservation of the basic biochemical properties of calponin from species to species suggests that these properties are relevant for its in vivo function. Its colocalization with actin and tropomyosin indicates that calponin is associated with the thin filament in intact smooth muscle cells.

Light and dark smooth muscle cells in estrogen-stimulated rat myometrium

1976 ◽  
Vol 54 (6) ◽  
pp. 822-833 ◽  
Author(s):  
R. E. Garfield ◽  
E. E. Daniel
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Atp Depletion ◽  
Metabolic Inhibitors ◽  
Volume Control ◽  
Control Mechanisms ◽  
Dark Cells ◽  
Light Cells

Smooth muscle cells of different densities to transmission of electrons (termed light and dark cells) were found in rat myometrium examined in the electron microscope following fixation by immersion in glutaraldehyde. Light cells accounted for about 4% of the total population of cells. No light cells were found in tissues fixed in situ by intraarterial perfusion with glutaraldehyde. In addition to staining differences, light cells were distinguished from most dark cells by differences in nuclear, mitochondrial, endoplasmic reticular, and surface structures. The relative number of light and dark cells after in vitro fixation was not changed in tissues relaxed with adrenaline or contracted with oxytocin. Mechanical injury resulted in increased numbers of light cells. Similarly, chemical injury with metabolic inhibitors resulted in ATP depletion, followed by increased numbers of light cells and gain in water content. We concluded that light cells were produced by mechanical or metabolic damage, leading to loss of volume control mechanisms, swelling, and leakage of protein. Light cells found after fixation in vitro in numerous prior studies represent cells damaged during isolation, and not a physiological variant among smooth muscle cells.

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