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PubMedDate not supplied

The effects of pathophysiologic state on the metabolism of vasoactive peptides by mammalian lung.

The pulmonary circulation plays a major role in the metabolism of angiotensin I (AI) and bradykinin through the activity of endothelial cell membrane-bound dipeptidylcarboxypeptidase, converting enzyme of kininase II. This report describes studies which investigate the effects of hypoxia on the function of converting enzyme in vivo in dogs and in endothelial cells in culture. Pulmonary converting enzyme function was assessed by both a blood pressure response technique and radioimmunoassay of bradykinin. Conversion of AI in vivo is decreased during acute alveolar hypoxia. At a PaO2 of 30 mmHg, conversion of AI is decreased to one-half control values. This decrease in AI conversion could not be related to hemodynamic factors in the pulmonary vasculature induced by hypoxia. Clearance of bradykinin by lung converting enzyme decreased from 96% at PaO2 levels above 95 torr to 0% below 26 torr. Hypoxic inhibition of enzyme activity was rapid in onset (less than 2 min), was closely correlated with PaO2 (r = 0.92, p less than 0.001) and reversible within 2 min after return to room air breathing. Converting enzyme activity of the systemic vascular bed also is inhibited by hypoxia. Converting enzyme activity also was studied by adding bradykinin or AI to endothelial cells in culture flasks and measuring residual peptide over time by radioimmunoassay. Hypoxia rapidly (less than 2 min) decreased enzyme activity and room air restored it rapidly. There was no enzyme activity below a PO2 of 30 mmHg. Hypoxia does not affect the activity of purified converting enzyme free of the endothelial cell. Metabolic and respiratory acidosis, as well as metabolic and respiratory alkalosis, had no significant effect on converting enzyme function in vivo in intact animals. While converting enzyme is resistant to a number of pathophysiological insults, it is extraordinarily responsive to acute hypoxia which may have important implications for systemic vasomotor control in conditions associated with clinical hypoxia and hypoxemia.

Acid-Base Equilibrium↗
PubMed2024

SCAR-6 elncRNA locus epigenetically regulates PROZ and modulates coagulation and vascular function.

In this study, we characterize a novel lncRNA-producing gene locus that we name Syntenic Cardiovascular Conserved Region-Associated lncRNA-6 (scar-6) and functionally validate its role in coagulation and cardiovascular function. A 12-bp deletion of the scar-6 locus in zebrafish (scar-6gib007Δ12/Δ12) results in cranial hemorrhage and vascular permeability. Overexpression, knockdown and rescue with the scar-6 lncRNA modulates hemostasis in zebrafish. Molecular investigation reveals that the scar-6 lncRNA acts as an enhancer lncRNA (elncRNA), and controls the expression of prozb, an inhibitor of factor Xa, through an enhancer element in the scar-6 locus. The scar-6 locus suppresses loop formation between prozb and scar-6 sequences, which might be facilitated by the methylation of CpG islands via the prdm14-PRC2 complex whose binding to the locus might be stabilized by the scar-6 elncRNA transcript. Binding of prdm14 to the scar-6 locus is impaired in scar-6gib007Δ12/Δ12 zebrafish. Finally, activation of the PAR2 receptor in scar-6gib007Δ12/Δ12 zebrafish triggers NF-κB-mediated endothelial cell activation, leading to vascular dysfunction and hemorrhage. We present evidence that the scar-6 locus plays a role in regulating the expression of the coagulation cascade gene prozb and maintains vascular homeostasis.

Animals↗
PubMed1978

Changes in the activity of the reticulo-endothelial system of rats during an infection with T. lewisi.

Data presented show that during the course of a Trypanosoma lewisi infection in rats there was both an activation of the phagocytic cells of the liver and spleen and an increase in their numbers. There was a marked lymphoid hyperplasia in the white pulp of the spleen with an increase in the number and size of the lymphoid follicles. Degenerative changes occurred in the liver parenchymal cells during the infection, and at certain stages large numgers of mononuclear cells were observed in the vascular sinusoids and other vessels of the liver.

Animals↗
PubMed1979

Effect of contact inhibition on the regulation of cholesterol metabolism in cultured vascular endothelial cells.

Cholesterol synthesis in actively growing bovine vascular endothelial cells is regulated by low density lipoprotein (LDL) at a step prior to mevalonate formation, in a manner comparable to that found in aortic smooth muscle cells. LDL uptake by these cells is associated with induction of cholesterol esterification, an increase in total cell cholesterol, and an inhibition of endogenous sterol synthesis. In contrast, cholesterol metabolism in confluent contact-inhibited endothelial cultures was not significantly affected by LDL even though the cells bind the lipoprotein at high affinity receptor sites. Lysosomal degradation and subsequent regulatory effects on cellular cholesterol metabolism, however, were observed in contact-inhibited endothelial cells incubated with cationized rather than native LDL. Cationized LDL enter the cells independently of the high affinity sites. Therefore, the primary regulation of cholesterol metabolism in these cells is neither through the appropriate intracellular enzymes nor through the high affinity surface receptors, but via an inhibition of LDL internalization. It is suggested that this inhibition is due to a strict contact-inhibited morphology which enables the endothelium of the larger arteries to function as a selective barrier to the high circulating levels of plasma LDL.

Animals↗
PubMed1978

Dexamethasone inhibition of experimental endothelial cell proliferation in retinal venules.

The observation that endothelial cell proliferation in retinal blood vessels is induced by ocular trauma in rats has been extended to mice. Indomethacin, 10 mg/kg/day, failed to block incorporation of tritiated thymidine into nuclei of venular endothelial cells in rat retinas observed 40 hr after puncturing the lens, but dexamethasone effectively suppressed tritiated thymidine incorporation, with 50% inhibition obtained with 0.2 mg/kg/day. The prostaglandin pathway does not appear essential to the activation of endothelial cell proliferation in this system.

Animals↗
PubMed1979

Lymphocyte migratory pathways in adjuvant disease. II. Distribution of thoracic duct lymph-borne immunoblasts.

Evidence for enhanced extravasation of thoracic duct lymph-borne immuno-blasts within joints of rats during the onset of adjuvant disease was sought by adoptive transfer of cells radiolabeled with (125I)-iodo-2-deoxyuridine. Migratory behavior of cells from normal or adjuvant disease donors, during both inductive and overt stages of the disease process, was contrasted in normal and adjuvant disease recipients. The results provided no evidence to indicate enhanced joint-seeking properties of lymph-borne immuno-blasts obtained from adjuvant disease donors, either during the period preceding overt joint involvement or during the phase of chronic inflammation. The ability of lymph-borne cells to passively transfer the disease thus appears more likely due to systemic actions of these cells, mediators produced by them, or concomitantly passaged antigen upon patterns of inflammatory cell mobilization and/or vascular endothelial cell activation.

Animals↗
PubMed1979

The ultrastructural features of laser trabeculopuncture and cyclodialysis. Problems related to successful treatment of chronic simple glaucoma.

Microexplosions induced by a Q-switched Nd:glass laser working above optical breakdown power density levels are able to destroy the inner wall of Schlemm's canal and to tear open both the supraciliary and suprachoroidal space. Furthermore, the ciliary muscles bundles may be disrupted, becoming subsequently permeable to the aqueous and thus also acting as a new outflow route. However, whereas breaks of the inner wall of Schlemm's canals are sealed in the monkey by the activity of endothelial cells forming a new Descemet membrane over the impact site, the supraciliary and suprachoroidal spaces remain open over an observation period of up to 480 days. Perfusion experiments with a HgS tracer substance have shown that these newly created, potential outflow routes may be considered as real additional filtration areas.

Animals↗
PubMed1976

[Appearance of phosphatase reticular cells in the spleen parenchyme of normal and tumor-bearing mice].

The splenic mouse parenchyma presents 3 reticular cells types revealed by histo-enzymatic technics: the phagocytic cells show a strong phosphatasic acid activity, the endothelial cells possess a phosphatasic alcalin or adenosine-triphosphatasic reaction, the perithelial cells are 5' nucleotidasic. These different cells are distributed by forming specific topographic structures in the splenic tissue. The phosphatasic alcalin reticular cells seem to be, with their distribution, characteristic elements of mouse spleen. Indeed the modifications in tumoral animal interest chiefly this cell category. In this case, the reticular cells form a deep and large membrane between marginal zone and perivascular lymphoid sheath of the white pulp. These different reticular cells probably react for the defense system of the animal.

Acid Phosphatase↗
PubMed1978

Electron microscopical studies on onchocerciasis. I. Mesenchyme reaction in untreated onchocercal dermatitis and ultrastructure of the microfilariae.

Skin biopsies of 22 untreated Liberian patients suffering from onchocercal dermatitis were studied by electron microscopy. The microfilariae tend to accumulate in the upper dermis, without eliciting a cellular reaction. Occasionally macrophages or mast cells are found in the neighbourhood of the microfilariae. The most conspicuous changes concern the presence of perivascular infiltrates, comprised of lymphocytes and macrophages, with a varying admixture of plasma cells. Only exceptionally the macrophages show an increase in number and size of their lysosomes and pseudopodia as well as prominent strands of ergastoplasm indicating an activation. The endothelial walls of the dermal vessels are swollen. The amount of mast cells in the upper dermis is increased. Ultrastructural features of the microfilariae are described, especially the cuticle, muscles, central undifferentiated cells and cephalic region. When comparing these findings with the literature on the fine structural morphology of the Latinamerican form, no differences can be found.

Adolescent↗
PubMed2002

Activation of Rac1 by shear stress in endothelial cells mediates both cytoskeletal reorganization and effects on gene expression.

Hemodynamic shear stress is a fundamental determinant of vascular remodeling and atherogenesis. Changes in focal adhesions, cytoskeletal organization and gene expression are major responses of endothelial cells to shear stress. Here, we show that activation of the small GTPase Rac is essential for gene expression and for providing spatial information for shear stress-induced cell alignment. Fluorescence resonance energy transfer (FRET) localizes activated Rac1 in the direction of flow. This directional Rac1 activation is downstream of shear-induced new integrin binding to extracellular matrix. Additionally, Rac1 mediates flow-induced stimulation of nuclear factor kappaB (NF-kappaB) and the subsequent expression of intercellular cell adhesion molecule 1 (ICAM-1), an adhesion receptor involved in the recruitment of leukocytes to atherosclerotic plaque. These studies provide a unifying model linking three of the main responses to shear stress that mediate both normal adaptation to hemodynamic forces and inflammatory dysfunction of endothelial cells in atherosclerosis.

Animals↗
PubMed1978

Fine structure of multiple neonatal haemangioendothelioma of the liver.

This paper discusses the fine structure of multiple haemangioendothelioma of the liver. There have been no previous reports of electron microscopic studies of this tumour, which was found to be composed of young capillaries continuous in type and varying in calibre. The capillaries were lined by actively proliferating, immature endothelial cells with pericytes forming an integral part of the tumour. Their morphological characteristics indicated intensive protein production. The authors suggest that the active pericytes play a role in the production of reticular fibres of the tumour. Following corticosteroid therapy, regression of tumour nodules occurred in this case in the interval between surgery and autopsy. This was confirmed by histological studies. The results seem to support the hypothesis that actively proliferating, young endothelial cells show an increased sensitivity to corticosteroids.

Basement Membrane↗
PubMed1976

Hyperreactive arterial endothelial cells: a clue for the treatment of atherosclerosis.

Arterial endothelial cells, which are capable of phagocytizing carbon particles of the same size as beta- and pre-beta-lipoprotein, were found only in endothelial cells of arterial segments susceptible to atheromatous changes in susceptible animal species, and the distribution closely corresponded to the susceptibility. The distribution of such endothelial cells is dense in large arteries, in the openings to their branches, especially in downstream portions, of rabbits, hens, and cocks; however, the distribution is relatively scanty in arteries of rhesus monkeys and is very scanty in dogs. Carbon particles were also rare in the suckling rabbit and tended to increase with age. They were not found in Wistar rats but were found in spontaneously hypertensive rats, which showed a characteristically diffuse distribution, even in relatively small arteries. The carbon particles, phagocytized, were released to the subendothelial space but were difficult to pass through the internal elastic lamina and tended to stagnate there for more than one month. The authors therefore call these cells hyperreactive endothelial cells. Various vasoactive substances, such as angiotensin II, histamine, and serotonin, significantly enhanced the phagocytic activities of arotic endothelial cells in rabbits; epinephrine and norepinephrine also slightly enhanced these activities. Various smooth muscle relaxants, such as ATP, pyridinol carbamate (ATP synthesis-enhancing substance), cycli-AMP, dibutyryl cycli-AMP, phthalazinol (cyclic-AMP phosphodiesterase inhibitor), iproveratril (calcium entry-inhibiting substance), colchicine, and vinblastine, with their different modes of action, commonly inhibited phagocytic activities, a finding that suggests a significant role for contractile protein in the permeability problem of atherogenesis. The atheromatous lesions of cholesterol-fed rabbits exhibited a striking increase in hyperreactive endothelial cells, accompanied by a marked rise in the activity of low-Km cyclic-AMP phosphodiesterase activity in atheromatous lesions and adjacent muscular layers, especially in rabbits with rapidly progressing atheroma.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1977

The endothelium: roles in thrombosis and hemostasis.

The renewed interest in endothelial function is based partly on success with tissue culture of endothelial cells. Endothelium functions primarily in the control of blood vessel wall permeability and in the provision of a blood-compatible lining surface. Recent findings indicate that endothelial cells are active metabolically in ways that may help prevent thrombosis. Endothelium actively degrades several different vasoactive compounds that circulate in blood and that can serve as platelet-aggregating agents. Endothelium also contains an inhibitor of platelet function and an activator of plasminogen, both of which can be released from the cell in response to appropriate stimuli. While intact endothelium functions primarily in prevention of thrombosis, damaged endothelium can contribute greatly to thrombus formation. Release of prostaglandins, adenine nucleotides, and other intracellular components from damaged endothelium can enhance platelet aggregation. Damaged endothelium may not function effectively in removal of vasoactive agents and may not release effective quantities of the inhibitor of platelet function or the activator of plasminogen. Altered endothelium exhibits tissue-factor activity, which can activate the extrinsic blood coagulation-system cascade. Finally, altered endothelial cells may contract and expose basement membrane to blood, thus enhancing thrombosis.

Blood Coagulation↗
PubMed1979

Cellular mechanics of dentinal bridge repair using 3H-thymidine.

Cellular reorganization in the pulp following mechanical pulp exposure involves three steps: First, lysis and macrophage resolution of the clot form; second, there is an invasion of the clot area by fibroblasts and endothelial cells, i.e., formation of granulation tissue; third, an organization and differentiation of these cells into functional odontoblasts occurs as early as 9 days after exposure. Autoradiographic results showed an increased DNA synthesis in the fibroblast and endothelial cell populations which coincided with a histologically-observed increase in those populations. A relative increase in fibroblastic activity, as compared to endothelial cell activity, suggested that fibroblasts may be the cells that replace odontoblasts.

Animals↗
PubMed1979

Lateral and transmembrane redistribution of tissue-specific antigens in single cells and monolayers.

Tissue-specific antigens in the membranes of corneal endothelial cells react with anti-tissue antibodies only in metabolically active monolayers and dispersed cells. After metabolic inhibition by exposure of these preparations to cold, the antigen-antibody complexes, like free antigens, undergo transmembrane redistribution leading to their internalization by the cells. This transmembrane redistribution is reversible and can be followed by using fluorescein-labeled antibodies. Reexpression of the complexes on the cell surfaces occurs after return from metabolic inhibition to metabolic activity. Dispersed corneal endothelial cells are also capable of lateral redistribution (capping) of the complexes although cells in monolayers do not share this capability. Capping in the dispersed cells occurs only at ambient temperatures and, because it results in shedding of the complexes, is irreversible. The data indicate that macromolecules in the membranes of cells organized in tissues are restricted in their movement as compared to the macromolecules of cells functioning in a dispersed state.

Animals↗
PubMed1977

Pseudopyogenic granuloma: enzyme histochemical and ultrastructural study.

In an attempt to elucidate the nature of the abnormal vessels in pseudopyogenic granuloma, we performed enzyme histochemical analysis of 10 lesions and correlated them with electron microscopic findings in four lesions. The dermal vessels of pseudopyogenic granuloma possess voluminous endothelial cells demonstrating marked activity of various hydrolytic and respiratory enzymes. The alkaline phosphatase activity, however, is characteristically faint or absent. Electron microscopy reveals that mitochondria and the other common cytoplasmic organelles are abundant in the hypertrophic endothelial cells, probably reflecting increased metabolic cellular activity, whereas specific endothelial granules (Weibel-Palade bodies) are generally sparse in these abnormal cells. Other notable features occurring in several endothelial cells are cytoplasmic vacuolation and the acquisition in the subnuclear zone of dense bodies associated with fine actin-like filaments, 55 to 75 A thick. The latter change is interpreted as evidence of endothelial contraction. Classification of the abnormal dermal vessels using available criteria has proved difficult, but it is suggested that they arise predominantly from the venous side of the microcirculation and are mainly postcapillary venules, although involvement of both larger and smaller caliber vessels also occurs.

Adenosine Triphosphatases↗
PubMed1978

Growth regulators in connective tissue. Systemic administration of an aortic extract inhibits tumor growth in mice.

A low-molecular-weight fraction prepared from extracts of bovine aorta inhibits the growth of a transplantable mammary tumor and a fibrosarcoma in mice when injected systemically. It also inhibits the growth of the fibrosarcoma in cell culture. The effect on the fibrosarcoma is much more marked than on the mammary tumor. Since the extract is more effective against the fibrosarcoma and is known to inhibit the growth of endothelial cells, it appears that the enhanced effect on this tumor is due to its activity on the endothelial cells of the host and the tumor cells themselves. The material injected is enriched in an antiproteinase we have previously isolated, which has anticollagneolytic activity and is presumed to be the effector molecule.

Animals↗