scholarly journals Production of proteolytic enzymes in mast cells, fibroblasts, vascular smooth muscle and endothelial cells cultivated under normoxic or hypoxic conditions

2010 ◽  
pp. 711-719 ◽  
Author(s):  
H Maxová ◽  
L Bačáková ◽  
V Lisá ◽  
J Novotná ◽  
H Tomášová ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Mast Cells ◽  
Vascular Smooth Muscle ◽  
Serine Proteases ◽  
Proteolytic Enzymes ◽  
Cell Types ◽  
In Vitro Production ◽  
Hypoxic Conditions

Matrix metalloproteinases (MMPs) is a family of proteolytic enzymes involved in remodeling of extracellular matrix. Although proteolytic enzymes are produced by many cell types, mast cells seem to be more important than other types in remodeling of pulmonary arteries during hypoxia. Therefore, we tested in vitro production of MMPs and serine proteases in four cell types (mast cells, fibroblasts, vascular smooth muscle cells and endothelial cells) cultivated for 48 h under normoxic or hypoxic (3 % O2) conditions. MMP-13 was visualized by immunohistochemistry, MMP-2 and MMP-9 were detected by zymography in cell lysates. Enzymatic activities (MMPs, tryptase and chymase) were estimated in the cultivation media. Hypoxia had a minimal effect on total MMP activity in the cultivation media of all types of cells, but immunofluorescence revealed higher intensity of MMP-13 in the cells exposed to hypoxia except of fibroblasts. Tryptase activity was three times higher and chymase activity twice higher in mast cells cultivated in hypoxia than in those cultured in normoxia. Among all cell types studied here, mast cells are the most abundant source of proteolytic enzymes under normoxic and hypoxic conditions. Moreover, in these cells hypoxia increases the production of both specific serine proteases tryptase and chymase, which can act as MMPs activators.

scholarly journals Omega-3 Fatty Acid-Derived Resolvin D2 Regulates Human Placental Vascular Smooth Muscle and Extravillous Trophoblast Activities

2019 ◽  
Vol 20 (18) ◽  
pp. 4402 ◽  
Author(s):  
Arzu Ulu ◽  
Prakash K. Sahoo ◽  
Ana G. Yuil-Valdes ◽  
Maheswari Mukherjee ◽  
Matthew Van Ormer ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Placental Tissue ◽  
Cell Types ◽  
Extravillous Trophoblast ◽  
Protective Effects ◽  
Omega 3 Fatty Acids ◽  
Omega 3

Omega-3 fatty acids are important to pregnancy and neonatal development and health. One mechanism by which omega-3 fatty acids exert their protective effects is through serving as substrates for the generation of specialized pro-resolving lipid mediators (SPM) that potently limit and resolve inflammatory processes. We recently identified that SPM levels are increased in maternal blood at delivery as compared to umbilical cord blood, suggesting the placenta as a potential site of action for maternal SPM. To explore this hypothesis, we obtained human placental samples and stained for the SPM resolvin D2 (RvD2) receptor GPR18 via immunohistochemistry. In so doing, we identified GPR18 expression in placental vascular smooth muscle and extravillous trophoblasts of the placental tissues. Using in vitro culturing, we confirmed expression of GPR18 in these cell types and further identified that stimulation with RvD2 led to significantly altered responsiveness (cytoskeletal changes and pro-inflammatory cytokine production) to lipopolysaccharide inflammatory stimulation in human umbilical artery smooth muscle cells and placental trophoblasts. Taken together, these findings establish a role for SPM actions in human placental tissue.

scholarly journals Hexamethylenebisacetamide selectively inhibits the proliferation of human and rat vascular smooth-muscle cells

1992 ◽  
Vol 283 (2) ◽  
pp. 403-408 ◽  
Author(s):  
D J Grainger ◽  
T R Hesketh ◽  
P L Weissberg ◽  
J C Metcalfe
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Cell Types ◽  
Maximal Inhibition ◽  
Vsmc Proliferation ◽  
Adp Ribosyltransferase

Hexamethylenebisacetamide (HMBA) selectively and reversibly inhibited proliferation of human and rat vascular smooth-muscle cells (VSMCs) compared with endothelial cells, fibroblasts or lymphocytes. Half-maximal inhibition of VSMC proliferation occurred at 2-5 mM-HMBA, and at 30- greater than 50 mM for other cell types. HMBA also prevented de-differentiation, defined by the loss of smooth-muscle-specific myosin heavy chain, of primary rat VSMCs and caused partial re-differentiation of subcultured cells. Other inhibitors of ADP-ribosyltransferase were also selective inhibitors of VSMC proliferation.

Determination of cell types and numbers during cardiac development in the neonatal and adult rat and mouse

2007 ◽  
Vol 293 (3) ◽  
pp. H1883-H1891 ◽  
Author(s):  
Indroneal Banerjee ◽  
John W. Fuseler ◽  
Robert L. Price ◽  
Thomas K. Borg ◽  
Troy A. Baudino
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Cardiac Development ◽  
Cardiac Fibroblasts ◽  
Cell Types ◽  
Cell Populations ◽  
Neonatal Development

Cardiac fibroblasts, myocytes, endothelial cells, and vascular smooth muscle cells are the major cellular constituents of the heart. The aim of this study was to observe alterations in myocardial cell populations during early neonatal development in the adult animal and to observe any variations of the cardiac cell populations in different species, specifically, the rat and mouse. Whole hearts were isolated from either mice or rats during the neonatal and adult stages of development, and single cell suspensions were prepared via sequential collagenase digestion. Heterogeneous cell populations were immunolabeled for specific cell types and analyzed using fluorescence-activated cell sorting (FACS). In addition, the left ventricle, right ventricle, and septa were isolated, fixed, and sectioned for morphometric analyses. These same cardiac regions were also analyzed using FACS. We observed that the adult murine myocardium is composed of ∼56% myocytes, 27% fibroblasts, 7% endothelial cells, and 10% vascular smooth muscle cells. Moreover, our morphometric and FACS data demonstrated similar percentages in the three regions examined. During murine neonatal cardiac development, we observed a marked increase in numbers of cardiac fibroblasts and a resultant decrease in percentages of myocytes in late neonatal development ( day 15). Finally, FACS analyses of the rat heart during development displayed similar results in relation to increases in cardiac fibroblasts during development; however, cell populations in the rat differed markedly from those observed in the mouse. Taken together, these data enabled us to establish a homeostatic model for the myocardium that can be compared with genetic and cardiac disease models.

Role of ephrinB2 expression in endothelial cells during arteriogenesis: impact on smooth muscle cell migration and monocyte recruitment

Blood ◽  
2008 ◽  
Vol 112 (1) ◽  
pp. 73-81 ◽  
Author(s):  
Thomas Korff ◽  
Jennifer Braun ◽  
Dennis Pfaff ◽  
Hellmut G. Augustin ◽  
Markus Hecker
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Cell Migration ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Cell Types ◽  
Cyclic Stretch ◽  
Smooth Muscle Cell Migration ◽  
The Impact

Abstract Expression of the arterial marker molecule ephrinB2 in endothelial cells is a prerequisite for adequate remodeling processes of the developing or angiogenic vasculature. Although its role in these processes has been extensively studied, the impact of ephrinB2 on the remodeling of adult arteries is largely unknown. To this end, we analyzed its expression during a biomechanically induced arteriolar remodeling process known as arteriogenesis and noted a significant increase in ephrinB2 expression under these conditions. By examining those biomechanical forces presumed to drive arteriogenesis, we identified cyclic stretch as a critical inducer of ephrinB2 expression in endothelial cells. Subsequent functional analyses in vitro revealed that endothelial cells expressing ephrinB2 limit the migration of smooth muscle cells, thereby enhancing segregation of both cell types. Moreover, MCP-1 induced transmigration of monocytes through a monolayer of endothelial cells overexpressing a truncated variant of ephrinB2 was clearly impeded. Taken together, these data suggest that expression of ephrinB2 in adult endothelial cells is up-regulated during arterial remodeling and controlled by cyclic stretch, a well-known inducer of such processes. This stretch-induced ephrinB2 expression may be pivotal for arteriogenesis as it limits smooth muscle cell migration within defined borders and controls monocyte extravasation.

Transfer and Expression of the Interferon Gamma Gene in Human Endothelial Cells Inhibits Vascular Smooth Muscle Cell Growth in Vitro

1997 ◽  
Vol 6 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Alison T. Stopeck ◽  
Mahmood Vahedian ◽  
Stuart K. Williams
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Cell Growth ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Interferon Gamma ◽  
Muscle Cell ◽  
Smooth Muscle Cell Growth

Intimal hyperplasia in blood vessels is primarily caused by the migration and proliferation of vascular smooth muscle cells. Excessive intimal thickening characterizes atherosclerosis as well as bypass graft and angioplasty failures. Endothelial cell-smooth muscle cell interactions and local cytokine production are important regulators of smooth muscle cell growth. Interferon gamma (γ-IFN), a product of T lymphocytes found in atherosclerotic lesions, inhibits smooth muscle cell proliferation in vitro. To determine if local delivery of γ-IFN may be useful in the treatment or prevention of vascular proliferative diseases, we transferred the human γ-IFN gene into endothelial cells isolated from human arteries and microvessels using a retroviral vector. Biologically active γ-IFN was produced and secreted by γ-IFN transduced endothelial cells, but not by control, nontransduced cells, or cells identically transduced with E. coli beta galactosidase (β-gal). To more closely approximate the microenvironment of blood vessels, subconfluent smooth muscle cells were plated in coculture with control, nontransduced endothelial cells, γ-IFN transduced endothelial cells, or β-gal transduced endothelial cells. Smooth muscle cell growth was inhibited 30-70% by coculture with γ-IFN transduced endothelial cells compared to coculture with β-gal transduced or control endothelial cells (p < 0.05). Our results suggest endothelial cells modified to produce γ-IFN may be a useful therapy in proliferative vascular diseases. Copyright © 1997 Elsevier Science Inc.

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