Endothelial and Smooth Muscle Cells as Antagonists in Vascular Fibrinoysis

1975 ◽  
Author(s):  
V. Noordhoek Hegt
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Blood Vessels ◽  
Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Vascular System ◽  
Muscle Cells ◽  
Vascular Wall ◽  
Vasa Vasorum ◽  
Slide Technique

Endothelial plasminogen activator activity in different types of human blood vessels obtained from fifty necropsies and thirty-five biopsies was detected and localized by means of plasminogen-rich fibrin slides. Great differences in endothelial activator activity were found along and across (vasa vasorum) the wall of the human vascular system.The same blood vessels were simultaneously investigated by a modified fibrin slide technique using plasminogen-free fibrin slides covered by plasmin to detect and localize inhibition of fibrinolysis in the vascular wall. The great variation in plasmin inhibition in different vessels revealed by this “fibrin slide sandwich technique” appeared to be closely associated with the localization and number of smooth muscle cells present in the walls of the vascular system. Strong plasmin inhibition was generally found at sites which showed no activator activity with the regular fibrin slide technique, while areas with a high endothelial fibrinolytic activity mostly revealed no inhibitory capacity.These results indicate that much of the variation in endothelial fibrinolytic activity on fibrin slides is due to inhibitory effects from the surrounding smooth muscle cells rather than to variability in the plasminogen activator content of the endothelium itself.

Persistence of Fibrinolytic Activity in Fragments of Human Veins Cultured in Vitro

1970 ◽  
Vol 24 (01/02) ◽  
pp. 043-047 ◽  
Author(s):  
M Pandolfi
Keyword(s):  
Blood Vessels ◽  
Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Vasa Vasorum ◽  
Adult Human ◽  
Slide Technique

SummaryExplants from 5 adult human veins were cultured in a fibrinolytically inactive medium for 3 weeks and assayed for the presence of plasminogen activator by the fibrin slide technique. The explants from 3 veins showed fibrinolytic activity confined to their vasa vasorum for the whole duration of the culture; no decrease of activity was seen. The finding suggests that small blood vessels are able to synthesize plasminogen activator.

Distribution of nitric oxide synthase activity in arterioles and venules of rat and human intestine

1994 ◽  
Vol 267 (2) ◽  
pp. G270-G275 ◽  
Author(s):  
K. Nichols ◽  
W. Staines ◽  
S. Rubin ◽  
A. Krantis
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Blood Vessels ◽  
Muscle Cells ◽  
Vascular Wall ◽  
Intestinal Wall ◽  
No Synthase ◽  
Human Intestine ◽  
Relative Contribution ◽  
Oxide Synthase

NO is produced within peripheral blood vessels through the action of the differentially distributed constitutive and inducible NO synthase isoforms in the vessel wall. As in other sites in the periphery, NO exerts local vasodilatory actions in the gastrointestinal microvasculature and is proposed to play a role in enteric vasomotor regulation. Using NO synthase histochemistry and endothelial cell immunohistochemistry, we provide the first anatomic evidence of NO synthesis in both endothelial and smooth muscle cells of submucosal blood vessels in the rat and human intestine. The findings of this study indicate that 1) as in the periphery, both the endothelial and vascular smooth muscle cells of the microvessels irrigating the rat and human intestinal wall possess NO synthesis potential, 2) NO synthase activity is predominantly localized to discrete subcellular patches, and 3) the source of NO within the vascular wall, either intimal or medial, should be a consideration in future studies in terms of the relative contribution of these sources of vasomotor tone in the rat and human gut wall.

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.

scholarly journals Role of Perivascular Adipose Tissue-Derived Adiponectin in Vascular Homeostasis

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1485
Author(s):  
Adrian Sowka ◽  
Pawel Dobrzyn
Keyword(s):  
Endothelial Cells ◽  
Adipose Tissue ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Vascular Wall ◽  
Whole Body ◽  
Perivascular Adipose Tissue

Studies of adipose tissue biology have demonstrated that adipose tissue should be considered as both passive, energy-storing tissue and an endocrine organ because of the secretion of adipose-specific factors, called adipokines. Adiponectin is a well-described homeostatic adipokine with metabolic properties. It regulates whole-body energy status through the induction of fatty acid oxidation and glucose uptake. Adiponectin also has anti-inflammatory and antidiabetic properties, making it an interesting subject of biomedical studies. Perivascular adipose tissue (PVAT) is a fat depot that is conterminous to the vascular wall and acts on it in a paracrine manner through adipokine secretion. PVAT-derived adiponectin can act on the vascular wall through endothelial cells and vascular smooth muscle cells. The present review describes adiponectin’s structure, receptors, and main signaling pathways. We further discuss recent studies of the extent and nature of crosstalk between PVAT-derived adiponectin and endothelial cells, vascular smooth muscle cells, and atherosclerotic plaques. Furthermore, we argue whether adiponectin and its receptors may be considered putative therapeutic targets.

Effect of all-trans retinoic acid and pentagalloyl glucose on smooth muscle cell elastogenesis

2021 ◽  
pp. 1-13
Author(s):  
Kaveh Sanaei ◽  
Sydney Plotner ◽  
Anson Oommen Jacob ◽  
Jaime Ramirez-Vick ◽  
Narendra Vyavahare ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Retinoic Acid ◽  
Smooth Muscle Cells ◽  
Blood Vessels ◽  
Muscle Cells ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Tissue Engineered Blood Vessels ◽  
Pentagalloyl Glucose ◽  
Vitamin A Derivative

BACKGROUND: The main objective of tissue engineering is to fabricate a tissue construct that mimics native tissue both biologically and mechanically. A recurring problem for tissue-engineered blood vessels (TEBV) is deficient elastogenesis from seeded smooth muscle cells. Elastin is an integral mechanical component in blood vessels, allowing elastic deformation and retraction in response to the shear and pulsatile forces of the cardiac system. OBJECTIVE: The goal of this research is to assess the effect of the vitamin A derivative all-trans retinoic acid (RA) and polyphenol pentagalloyl glucose (PGG) on the expression of elastin in human aortic smooth muscle cells (hASMC). METHODS: A polycaprolactone (PCL) and the gelatin polymer composite was electrospun and doped with RA and PGG. The scaffolds were subsequently seeded with hASMCs and incubated for five weeks. The resulting tissue-engineered constructs were evaluated using qPCR and Fastin assay for their elastin expression and deposition. RESULTS: All treatments showed an increased elastin expression compared to the control, with PGG treatments showing a significant increase in gene expression and elastin deposition.

scholarly journals Extrarenal angiomyolipoma in uterine cervix: rare presentation in unusual site

2019 ◽  
Vol 8 (1) ◽  
pp. 367
Author(s):  
Rashmi Monteiro ◽  
Shikha Sharma ◽  
Sonal Gupta ◽  
Indu Choudhary
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Blood Vessels ◽  
Uterine Cervix ◽  
Abdominal Mass ◽  
Muscle Cells ◽  
Renal Angiomyolipoma ◽  
Rare Presentation ◽  
Unusual Site ◽  
Hmb 45

Angiomyolipoma is a benign neoplasm composed of variable admixture of blood vessels, smooth muscle cells and adipose tissue. Cervical angiomyolipoma are extremely rare and to the best of our knowledge only five cases of angiomyolipoma in cervix have been reported in the literature till date. Authors are presenting a case of angiomyolipoma arising from the uterine cervix. 43 years old female presented with mass descending per vagina for 6 months. This case had no association with tuberous sclerosis. Microscopic examination showed an ill-defined polypoidal, non-encapsulated lesion covered by keratinized stratified epithelium. The lesion is made up of three components, predominantly by fascicles of spindle shaped cells, varying sized blood vessels and multiple foci of mature adipocytes with no evidence of atypia or increased mitotic activity. Smooth muscle component showed strong immunoreactivity to SMA and absence of elastic fibres in the blood vessels were confirmed by histochemistry. Non-vascular smooth muscle cells were negative for HMB-45 in contrast to renal and other extra-renal angiomyolipoma in which HMB-45 immunoreactivity in seen in these cells. To conclude, the differential diagnosis of lower abdominal mass and dysfunctional uterine bleeding should include the angiomyolipoma, even though the uterine cervix is an extremely rare location where they occur.

ANG II increases TIMP-1 expression in rat aortic smooth muscle cells in vivo

2003 ◽  
Vol 284 (2) ◽  
pp. H635-H643 ◽  
Author(s):  
Giovanna Castoldi ◽  
Cira R. T. di Gioia ◽  
Federico Pieruzzi ◽  
Cristina D'Orlando ◽  
Willy M. M. van de Greef ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Vascular Wall ◽  
Dependent Manner ◽  
Ang Ii ◽  
Maximal Increase ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle

Matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) are involved in tissue remodeling processes. TIMP-1 is the main native inhibitor of MMPs and it contributes to the development of tissue fibrosis. It is known that ANG II plays a fundamental role in vascular remodeling. In this study, we investigated whether ANG II modulates TIMP-1 expression in rat aortic smooth muscle cells. In vitro, ANG II induces TIMP-1 mRNA expression in a dose-dependent manner. The maximal increase in TIMP-1 expression was present after 3 h of ANG II stimulation. The ANG II increase in TIMP-1 expression was mediated by the ANG type 1 receptors because it was blocked by losartan. The increase in TIMP-1 expression was present after the first ANG II treatment, whereas repeated treatments (3 and 5 times) did not modify TIMP-1 expression. In vivo, exogenous ANG II was administered to Sprague-Dawley rats (200 ng · kg−1· min−1sc) for 6 and 25 days. Control rats received physiological saline. After treatment, systolic blood pressure was significantly higher ( P < 0.01), whereas plasma renin activity was suppressed ( P < 0.01), in ANG II-treated rats. ANG II increased TIMP-1 expression in the aorta of ANG II-treated rats both at the mRNA ( P < 0.05) and protein levels as evaluated by Western blotting ( P < 0.05) and/or immunohistochemistry. Neither histological modifications at the vascular wall nor differences in collagen content in the tunica media were present in both the ANG II- and saline-treated groups. Our data demonstrate that ANG II increases TIMP-1 expression in rat aortic smooth muscle cells. In vivo, both short- and long-term chronic ANG II treatments increase TIMP-1 expression in the rat aorta. TIMP-1 induction by ANG II in aortic smooth muscle cells occurs in the absence of histological changes at the vascular wall.

LRP and αvβ3 mediate tPA activation of smooth muscle cells

2006 ◽  
Vol 291 (3) ◽  
pp. H1351-H1359 ◽  
Author(s):  
Sa'ed Akkawi ◽  
Taher Nassar ◽  
Mark Tarshis ◽  
Douglas B. Cines ◽  
Abd Al-Roof Higazi
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Plasminogen Activator ◽  
Vascular Smooth Muscle Cells ◽  
Density Lipoprotein ◽  
Plasminogen Activator Inhibitor ◽  
Muscle Cells ◽  
Tissue Type ◽  
Pai 1

Tissue-type plasminogen activator (tPA) regulates vascular contractility through the low-density lipoprotein-related receptor (LRP), and this effect is inhibited by plasminogen activator inhibitor type 1 (PAI-1). We now report that tPA-mediated vasocontraction also requires the integrin αvβ3. tPA-induced contraction of rat aortic rings is inhibited by the Arg-Gly-Asp (RGD) peptide and by monoclonal anti-αvβ3 antibody. tPA induces the formation of a complex between LRP and αvβ3 in vascular smooth muscle cells. The three proteins are internalized within 10 min, causing the cells to become refractory to the readdition of tPA. LRP and αvβ3 return to the cell surface by 90 min, restoring cell responsiveness to tPA. PAI-1 and the PAI-1-derived hexapeptide EEIIMD abolish the vasocontractile activity of tPA and inhibit the tPA-mediated interaction between LRP and αvβ3. tPA induces calcium mobilization from intracellular stores in vascular smooth muscle cells, and this effect is inhibited by PAI-1, RGD, and antibodies to both LRP and αvβ3. These data indicate that tPA-mediated vasocontraction involves the coordinated interaction of LRP with αvβ3. Delineating the mechanism underlying these interactions and the nature of the signals transduced may provide new tools to regulate vascular tone and other consequences of tPA-mediated signaling.

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