scholarly journals Endothelial cells and not smooth muscle cells are affected during a photodynamic therapy of atherosclerotic plaques

1991 ◽  
Vol 17 (6) ◽  
pp. 1446-1447
Author(s):  
J.T. Beranek
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Photodynamic Therapy ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Atherosclerotic Plaques

Abstract 353: Elastase-Activated Stress Response of Vascular Cells

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Irina Grechowa ◽  
Bernhard Dorweiler ◽  
Anja Wallrath ◽  
Sven Horke
Keyword(s):  
Flow Cytometry ◽  
Endothelial Cells ◽  
Cell Death ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Apoptotic Cell ◽  
Muscle Cells ◽  
Apoptotic Cell Death ◽  
Atherosclerotic Plaques ◽  
Vascular Cells

Introduction: Rupture of atherosclerotic plaques is the most abundant cause for stroke. The serine protease elastase plays an important role as it induces death of endothelial cells (ECs) and smooth muscle cells (SMCs), and breaks down the fibrous cap of atherosclerotic plaques. Increased elastase concentrations were found in patients with symptomatic stenosis. We previously showed that elastase activates the endoplasmic reticulum (ER) stress signaling pathway unfolded protein response (UPR) in rupture-prone plaques of human carotid artery. However, signaling pathways elicited by elastase in vascular cells were largely unknown. We hypothesized that elastase induces cell-type dependent responses in ECs, SMCs and macrophages (M[[Unable to Display Character: &#1060;]]). Methods and Results: Different forms of cell death and UPR activation were analyzed in primary and immortalized endothelial cells, coronary artery smooth muscle cells (HCASMCs) and M[[Unable to Display Character: &#1060;]] after treatment with human neutrophil elastase. To discriminate between the involved cell death types, three independent assays were performed. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-assay by confocal microscopy (p < .01), caspase3/7 activity by chemiluminescence-assays (p < .01) and cell-cycle analysis by flow cytometry revealed that an autophagic/apoptotic cell death was induced upon elastase treatment. This appeared specific for ECs, as it was absent in M[[Unable to Display Character: &#1060;]]. Necrosis (as determined by chemiluminescent lactate dehydrogenase-release assay) and necroptosis (assessed by flow cytometry) played only minor roles. The involvement of the UPR was investigated on protein and / or gene expression level. The high levels of GRP78, phospho-PERK, phospho-eIF2α, spliced XBP1 and CHOP indicate a strongly activated UPR that may give rise to the subsequent induced autophagic/apoptotic cell death. Conclusion: Elastase plays a significant role in plaque stability and cell survival likely through activation of a UPR/autophagic type of endothelial cell death. This may explain underlying molecular links how elastase destabilizes atherosclerotic plaques.

scholarly journals Pathogenesis of atherosclerosis in the tunica intima, media, and adventitia of coronary arteries: An updated review

2019 ◽  
Author(s):  
Aleksandra Milutinović ◽  
Dušan Šuput ◽  
Ruda Zorc-Pleskovič
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Coronary Arteries ◽  
Muscle Cells ◽  
Chronic Inflammatory Disease ◽  
Elastic Membrane ◽  
Atherosclerotic Plaques ◽  
Perivascular Adipose Tissue ◽  
Tunica Intima

Atherosclerosis is a chronic inflammatory disease of arteries and it affects the structure and function of all three layers of the coronary artery wall. Current theories suggest that the dysfunction of endothelial cells is one of the initial steps in the development of atherosclerosis. The view that the tunica intima normally consists of a single layer of endothelial cells attached to the subendothelial layer and internal elastic membrane has been questioned in recent years. The structure of intima changes with age and it becomes multilayered due to migration of smooth muscle cells from the media to intima. At this stage, the migration and proliferation of smooth muscle cells do not cause pathological changes in the intima. The multilayering of intima is classically considered to be an important stage in the development of atherosclerosis, but in fact atherosclerotic plaques develop only focally due to the interplay of various processes that involve the resident and invading inflammatory cells. The tunica media consists of multiple layers of smooth muscle cells that produce the extracellular matrix, and this layer normally does not contain microvessels. During the development of atherosclerosis, the microvessels from the tunica adventitia or from the lumen may penetrate thickened media to provide nutrition and oxygenation. According to some theories, the endothelial dysfunction of these nutritive vessels may significantly contribute to the atherosclerosis of coronary arteries. The adventitia contains fibroblasts, progenitor cells, immune cells, microvessels, and adrenergic nerves. The degree of inflammatory cell infiltration into the adventitia, which can lead to the formation of tertiary lymphoid organs, correlates with the severity of atherosclerotic plaques. Coronary arteries are surrounded by perivascular adipose tissue that also participates in the atherosclerotic process.

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

1994 ◽  
Vol 72 (01) ◽  
pp. 044-053 ◽  
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.

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

1982 ◽  
Vol 48 (01) ◽  
pp. 101-103 ◽  
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.

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

1985 ◽  
Vol 53 (02) ◽  
pp. 165-169 ◽  
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.

Endothelial Cells Inhibit NO Generation by Vascular Smooth Muscle Cells

1996 ◽  
Vol 16 (10) ◽  
pp. 1263-1268 ◽  
Author(s):  
Antonio López Farré ◽  
Juan R. Mosquera ◽  
Lourdes Sánchez de Miguel ◽  
Inmaculada Millás ◽  
Trinidad de Frutos ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells
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