Stimulus and cell-specific expression of C-X-C and C-C chemokines by pulmonary stromal cell populations

Chronic inflammatory responses in the lung rely on the continual recruitment of leukocytes to the site of inflammation. Recent data have demonstrated a possible role for stromal cell-derived chemokines in leukocyte recruitment. In the present study we examined the production of interleukin (IL)-8 and ENA-78, members of the C-X-C family of chemokines, and macrophage inflammatory protein (MIP)-1 alpha and MIP-1 beta, members of the C-C chemokine family, from pulmonary smooth muscle and endothelial cells. The production of IL-8 and ENA-78 was induced by early response cytokines, IL-1 and tumor necrosis factor (TNF), but not by immune-associated cytokines, IL-4, IL-10, or interferon (IFN)-gamma. In contrast, the production of MIP-1 alpha and MIP-1 beta by pulmonary vascular smooth muscle cells increased when stimulated by immune-associated cytokines as well as with IL-1 beta and TNF. The level of MIP-1 alpha production induced in smooth muscle cells by the immune-associated cytokines, IL-4, IFN-gamma, and IL-10 ranged from 0 to 340 pg/ml. The production of MIP-1 beta in response to the immune-associated cytokines IL-4, IFN-gamma, and IL-10 in smooth muscle cells ranged from 260 to 940 pg/ml. Human pulmonary artery endothelial cells did not generate MIP-1 alpha or MIP-1 beta in response to graded doses of any of the cytokines. These data demonstrate differential induction of C-X-C and C-C chemokines from nonimmune stromal cell populations.(ABSTRACT TRUNCATED AT 250 WORDS)

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Abstract WMP31: Dedifferentiation of Smooth Muscle Cells and its Potential Contribution to Pathogenesis of Intracranial Aneurysms

Stroke ◽

10.1161/str.51.suppl_1.wmp31 ◽

2020 ◽

Vol 51 (Suppl_1) ◽

Author(s):

Mieko Oka ◽

Nobuhiko Ohno ◽

Takakazu Kawamata ◽

Tomohiro Aoki

Keyword(s):

Endothelial Cells ◽

Smooth Muscle ◽

Smooth Muscle Cells ◽

Inflammatory Responses ◽

Muscle Cells ◽

Inflammatory Factors ◽

Potential Contribution ◽

Electron Microscopic

Introduction: Intracranial aneurysm (IA) affects 1 to 5 % in general public and becomes the primary cause of subarachnoid hemorrhage, the most severe form of stroke. However, currently, no drug therapy is available for IAs to prevent progression and rupture of lesions. Elucidation of mechanisms underlying the disease is thus mandatory. Considering the important role of vascular smooth muscle cells (SMCs) in the maintenance of stiffness of arterial walls and also in the pathogenesis of atherosclerosis via mediating inflammatory responses, we in the present study analyzed morphological or phenotypical changes of SMCs during the disease development in the lesions. Methods: We subjected rats to an IA model in which lesions are induced by increase of hemodynamic force loading on intracranial arterial bifurcations and performed histopathological analyses of induced lesions including the electron microscopic examination. We then immunostained specimens from induced lesions to explore factors responsible for dedifferentiation or migration of SMCs. In vitro study was also done to examine effect of some candidate factors on dedifferentiation or migration of cultured SMCs. Results: We first found the accumulation of SMCs underneath the endothelial cell layer mainly at the neck portion of the lesion. These cells was positive for the embryonic form of myosin heavy chain, a marker for the dedifferentiated SMCs, and the expression of pro-inflammatory factors like TNF-α. In immunostaining to explore the potential factor regulating the dedifferentiation of SMCs, we found that Platelet-derived growth factor-BB (PDGF-BB) was expressed in endothelial cells at the neck portion of IA walls. Consistently, recombinant PDGF-BB could promote the dedifferentiate of SMCs and chemo-attracted them in in vitro. Finally, in the stenosis model of the carotid artery, PDGF-BB expression was induced in endothelial cells in which high wall shear stress was loaded and the dedifferentiation of SMCs occurred there. Conclusions: The findings from the present study imply the role of dedifferentiated SMCs partially recruited by PDGF-BB from endothelial cells in the formation of inflammatory microenvironment at the neck portion of IA walls, leading to the progression of the disease.

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Complexity of Inflammatory Responses in Endothelial Cells and Vascular Smooth Muscle Cells Determined by Microarray Analysis

Annals of the New York Academy of Sciences ◽

10.1111/j.1749-6632.2002.tb05943.x ◽

2002 ◽

Vol 975 (1) ◽

pp. 77-90 ◽

Cited By ~ 34

Author(s):

OLGA BANDMAN ◽

ROGER T. COLEMAN ◽

JEANNE F. LORING ◽

JEFFREY J. SEILHAMER ◽

BENJAMIN G. COCKS

Keyword(s):

Endothelial Cells ◽

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Smooth Muscle Cells ◽

Microarray Analysis ◽

Vascular Smooth Muscle Cells ◽

Inflammatory Responses ◽

Muscle Cells

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Influence of conjugated linoleic acids on functional properties of vascular cells

British Journal Of Nutrition ◽

10.1017/s0007114509990304 ◽

2009 ◽

Vol 102 (8) ◽

pp. 1099-1116 ◽

Cited By ~ 5

Author(s):

Robert Ringseis ◽

Klaus Eder

Keyword(s):

Endothelial Cells ◽

Smooth Muscle ◽

Smooth Muscle Cells ◽

Functional Properties ◽

Inflammatory Responses ◽

Atherosclerotic Lesion ◽

Muscle Cells ◽

Vascular Wall ◽

Mechanisms Of Action ◽

Conjugated Linoleic Acids

Conjugated linoleic acids (CLA) are biologically highly active lipid compounds that inhibit the development of atherosclerotic plaques in experimental animals. The underlying mechanisms of action, however, are only poorly understood. Since cell-culture experiments are appropriate to provide a detailed view into the mechanisms of action of a compound, the present review summarises results from in vitro studies dealing with the effects of CLA isomers and CLA mixtures on functional properties of cells of the vascular wall, such as endothelial cells, smooth muscle cells and monocyte-derived macrophages, which are amongst the major cells contributing to atherosclerotic lesion development. Based on these studies, it can be concluded that CLA exert several beneficial actions in cells of the vascular wall through the activation of nuclear PPAR. These actions of CLA, which may, at least partially, explain the inhibition of atherogenesis by dietary CLA, include modulation of vasoactive mediator release from endothelial cells, inhibition of inflammatory and fibrotic processes in activated smooth muscle cells, abrogation of inflammatory responses in activated macrophages, and reduction of cholesterol accumulation in macrophage-derived foam cells.

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Cell specific expression of Sphingosine‐1‐Phosphate receptors in endothelial cells and smooth muscle cells

The FASEB Journal ◽

10.1096/fasebj.22.1_supplement.1145.5 ◽

2008 ◽

Vol 22 (S1) ◽

Author(s):

Nicola K Hudson ◽

Paul F Speake ◽

Nicola J Robinson ◽

Philip N Baker ◽

Michael J Taggart

Keyword(s):

Endothelial Cells ◽

Smooth Muscle ◽

Smooth Muscle Cells ◽

Muscle Cells ◽

Specific Expression ◽

Sphingosine 1 Phosphate

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Cell-specific expression and function of IKCa channels in cerebral endothelial cells but not smooth muscle cells: Relevance to the mechanism of EDHF-mediated dilation

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/sj.jcbfm.9591524.0201 ◽

2005 ◽

Vol 25 (1_suppl) ◽

pp. S201-S201

Author(s):

Christina Hatfield ◽

Marrelli Sean

Keyword(s):

Endothelial Cells ◽

Smooth Muscle ◽

Smooth Muscle Cells ◽

Muscle Cells ◽

Specific Expression ◽

Cerebral Endothelial Cells ◽

And Function

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Plasminogen Activator Inhibitor-1 Expression in Human Liver and Healthy or Atherosclerotic Vessel Walls

Thrombosis and Haemostasis ◽

10.1055/s-0038-1648809 ◽

1994 ◽

Vol 72 (01) ◽

pp. 044-053 ◽

Cited By ~ 76

Author(s):

N Chomiki ◽

M Henry ◽

M C Alessi ◽

F Anfosso ◽

I Juhan-Vague

Keyword(s):

Endothelial Cells ◽

Smooth Muscle ◽

Smooth Muscle Cells ◽

Plasminogen Activator ◽

Human Liver ◽

Plasminogen Activator Inhibitor ◽

Muscle Cells ◽

Vessel Walls ◽

Activator Inhibitor ◽

Pai 1

SummaryIndividuals with elevated levels of plasminogen activator inhibitor type 1 are at risk of developing atherosclerosis. The mechanisms leading to increased plasma PAI-1 concentrations are not well understood. The link observed between increased PAI-1 levels and insulin resistance has lead workers to investigate the effects of insulin or triglyceride rich lipoproteins on PAI-1 production by cultured hepatocytes or endothelial cells. However, little is known about the contribution of these cells to PAI-1 production in vivo. We have studied the expression of PAI-1 in human liver sections as well as in vessel walls from different territories, by immunocytochemistry and in situ hybridization.We have observed that normal liver endothelial cells expressed PAI-1 while parenchymal cells did not. However, this fact does not refute the role of parenchymal liver cells in pathological states.In healthy vessels, PAI-1 mRNA and protein were detected primarily at the endothelium from the lumen as well as from the vasa vasorum. In normal arteries, smooth muscle cells were able to produce PAI-1 depending on the territory tested. In deeply altered vessels, PAI-1 expression was observed in neovessels scattering the lesions, in some intimal cells and in smooth muscle cells. Local increase PAI-1 mRNA described in atherosclerotic lesions could be due to the abundant neovascularization present in the lesion as well as a raised expression in smooth muscle cells. The increased PAI-1 in atherosclerosis could lead to fibrin deposit during plaque rupture contributing further to the development and progression of the lesion.

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Thrombin Inhibition and Thrombin Generation by Cultured Aortic Endothelial and Smooth Muscle Cells from Minipig

Thrombosis and Haemostasis ◽

10.1055/s-0038-1657227 ◽

1982 ◽

Vol 48 (01) ◽

pp. 101-103 ◽

Cited By ~ 1

Author(s):

B Kirchhof ◽

J Grünwald

Keyword(s):

Endothelial Cells ◽

Smooth Muscle ◽

Smooth Muscle Cells ◽

Vessel Wall ◽

Thrombin Generation ◽

Muscle Cells ◽

Thrombin Inhibition ◽

Generating Capacity ◽

Wall Interaction ◽

Cells Cultured

SummaryEndothelial and smooth muscle cells cultured from minipig aorta were examined for their inhibitory activity on thrombin and for their thrombin generating capacity.Endothelial cells showed both a thrombin inhibition and an activation of prothrombin in the presence of Ca++, which was enhanced in the presence of phospholipids. Smooth muscle cells showed an activation of prothrombin but at a lower rate. Both coagulation and amidolytic micro-assays were suitable for studying the thrombin-vessel wall interaction.

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Vascular Smooth Muscle Cells Inhibit the Plasminogen Activators Secreted by Endothelial Cells

Thrombosis and Haemostasis ◽

10.1055/s-0038-1661265 ◽

1985 ◽

Vol 53 (02) ◽

pp. 165-169 ◽

Cited By ~ 24

Author(s):

Walter E Laug

Keyword(s):

Endothelial Cells ◽

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Smooth Muscle Cells ◽

Conditioned Medium ◽

Vascular Smooth Muscle Cells ◽

Inhibitory Activity ◽

Muscle Cells ◽

Plasminogen Activators ◽

Bovine Endothelial Cells

SummaryTPure cultures of bovine endothelial cells (EC) produce and secrete large amounts of plasminogen activators (PA). Cocultivation of EC with vascular smooth muscle cells (SMC) resulted in a significant decrease of PA activities secreted by the EC, whereas the cellular PA activities remained unaffected. Secreted PA activities were absent in the growth medium as long as the SMC to EC ratio was 2:1 or higher. The PA inhibitory activity of the SMC was rapid and cell-to-cell contact was not necessary.The PA inhibitory activity was present in homogenates of SMC as well as in the medium conditioned by them but not in the extracellular matrix elaborated by these cells. Serum free medium conditioned by SMC neutralized both tissue type (t-PA) and urokinase like (u-PA) plasminogen activators. Gel electrophoretic analysis of SMC conditioned medium followed by reverse fibrin autography demonstrated PA inhibitory activities in the molecular weight (Mr) range of 50,000 to 52,000 similar to those present in media conditioned by bovine endothelial cells or fibroblasts. Regular fibrin zymography of SMC conditioned medium incubated with u-PA or t-PA revealed the presence of a component with a calculated approximate Mr of 45,000 to 50,000 which formed SDS resistant complexes with both types of PA.These data demonstrate that vascular SMC produce and secrete (a) inhibitor(s) of PAs which may influence the fibrinolytic potential of EC.

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