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Biomedical subjects

J D Pearson

Publications and source records attributed to J D Pearson.

At least 217 records · Page 12Linked to original sources
PubMed1980

Metabolism of adenine nucleotides by ectoenzymes of vascular endothelial and smooth-muscle cells in culture.

1. Pig aortic endothelial and smooth-muscle cells in culture rapidly catabolize exogenous ATP, ADP or AMP. 2. In both cell types catabolism is due to Mg2+-stimulated ectoenzymes. 3. Inhibition and substrate-specificity studies suggest that both cell types possess three distinct ectonucleotidases, namely nucleoside triphosphatase (EC 3.6.1.15), nucleoside diphosphatase (EC 3.6.1.6) and 5'-nucleotidase (EC 3.1.3.5), as well as nucleoside diphosphate kinase (EC 2.7.4.6). 4. These ectonucleotidase systems could be of importance in the regulation of neurotransmission, blood platelet function and vasodilation.

Acid Anhydride Hydrolases↗
PubMed1979

Vascular endothelial and smooth muscle cells in culture selectively release adenine nucleotides.

Endothelial cells in culture can modulate platelet aggregation and vascular tone, in part by producing prostacyclin (PGI2), a powerful vasodilator and inhibitor of platelet aggregation, but also by their ecto-ADPase activity, which initiates the conversion of pro-aggregating ADP to adenosine, a potent vasodilator and platelet inhibitor. We have now demonstrated that cultured aortic endothelial cells exposed to trypsin, thrombin or other stimuli can liberate a high proportion of their adenine nucleotides without substantial loss of lactate dehydrogenase. ADP rapidly accumulates extracellularly, reaching biologically active concentrations before there is further breakdown to adenosine. Whether this selective release of nucleotides is a response to damage, or whether it represents a specific secretory mechanism remains to be resolved. Cultured aortic smooth muscle cells can secrete adenine nucleotides in a similar manner, but extracellular conversion to adenosine occurs much faster.

Adenine Nucleotides↗
PubMed1979

Stimulation of lymphocyte proliferation by non-lymphoid porcine tissue cells.

Cultured porcine non-lymphoid cells, characterized by biochemical and morphological criteria, were derived from different tissues of individuals typed by serological and mixed lymphocyte culture methods for gene products of the major histocompatibility complex. These cultured cells have been used as stimulators in mixed lymphocyte-tissue cell cultures in order to investigate (1) the magnitude, kinetics and dose-dependence of lymphocyte transformation caused by tissue cells compared with that caused by lymphocytes as stimulators; (2) the relationship between the expression of serologically detected Ia-like antigens by tissue cells and their ability to cause lymphocyte transformation; (3) the genetic control of stimulation by tissue cells and by lymphocytes and (4) the expression and genetic control of lymphocyte stimulatory properties restricted to tissue cells and absent from lymphocytes. It has been shown that some but not all kinds of tissue cells can stimulate allogeneic lymphocytes strongly and that the characteristics of such stimulation are similar to those observed in mixed lymphocyte cultures. Strong stimulation by tissue cells does not always correlate with the expression of serologically detectable Ia-like antigens, but appears to be controlled by the major histocompatibility complex. There is evidence that certain tissue cells possess lymphocyte stimulatory properties not shared by lymphocytes. Preliminary data suggest that such tissue cell specific stimulation is not controlled by the major histocompatibility complex, though more detailed genetic analysis is required.

Animals↗
PubMed1979

Granulocyte adhesion to endothelium in culture.

We previously described a model system for studying the adherence of granulocytes to cultured endothelium, and have now investigated the effects of other blood components on granulocyte adhesion in this system. Red cells enhanced adhesion, whereas blood platelets decreased adhesion, and further experiments suggested that endothelial cells secrete a proadhesive factor, particularly if incubated with plasma. We have also investigated the effects of several drugs, and attempted to localize their sites of action. Flavonoid drugs increased adhesion by an effect at the endothelial cell surface, whereas agents that increase cyclic AMP levels, including several prostaglandins, stimulated adhesion mainly by their effects on granulocytes. The effects of some agents on granulocyte adhesion to endothelium were not paralleled by their effects on adhesion to serum-coated glass. We conclude that granulocyte-endothelial interaction is a complex process, with each cell type responding to the other or to factors produced by it, and that data derived solely from studies of granulocyte adhesion to inert substrata will not always reflect granulocyte-endothelial interaction in vivo.

Animals↗
PubMed1979

Granulocyte migration through endothelium in culture.

Using a model system with which we have previously investigated the adhesion of granulocytes to cultured endothelium, we have now shown that adherent granulocytes migrate through cultured endothelium in a manner closely resembling that found during the acute inflammatory response in vivo. The migration of granulocytes was markedly enhanced in the presence of erythrocytes, whereas blood platelets did not affect migration. Several test agents, including Paroven and some prostaglandins, had different effects upon migration and adhesion. We conclude that the adhesion of granulocytes to endothelium and their migration through it are responses that are, at least in part, separately controlled, and that migration does not depend exclusively upon extravascular stimuli.

Animals↗
PubMed1978

Uptake and metabolism of adenosine by pig aortic endothelial and smooth-muscle cells in culture.

1. Adenosine, a potent vasodilator, is transported very efficiently by pig aortic endothelium in monolayer culture (approx. 50pmol/min per 10(6) cells at 2 micrometer). Uptake proceeds by diffusion at high (millimolar) substrate concentrations, and by two discrete transport processes (Km approx. 3 micrometer and 250 micrometer) at lower concentrations. Over 90% of the adenosine taken up at 10 micrometer or 100 micrometer is rapidly converted into adenine nucleotides (mainly ATP). 2. The high-affinity process is selectively inhibited by dipyridamole and by nitrobenzylthioinosine. Adenine preferentially inhibits the lower-affinity process, papapaverine inhibits both transport processes, and inosine has no significant effect. 3. Pig aortic smooth-muscle cells in culture show no high-affinity transport system for adenosine; uptake is much slower at low concentrations than that by endothelium (approx. 5pmol/min per 10(6) cells at 2 micrometer). Over 80% of the incorporated adenosine at 10 micrometer or 100 micrometer is rapidly converted into adenine nucleotides. 4. The uptake of adenosine by smooth-muscle cells is powerfully inhibited by adenine, but dipyridamole is much less potent than in endothelium. 5. We conclude that endothelial cells are mainly responsible for the removal of circulating adenosine.

Adenine↗
PubMed1978

Effects of sulphinpyrazone and aspirin on prostaglandin I2 (prostacyclin) synthesis by endothelial cells.

Synthesis of prostaglandin I2, (PGI2, prostacyclin) by vascular endothelium (assayed by the ability of cultured endothelial cells to inhibit platelet aggregation) was inhibited by aspirin. At 100 mumol/l aspirin completely blocked measurable PGI2 production, but endothelial cells had substantially recovered their ability to synthesize PGI2 24 h after removal of the drug. In contrast, the effect of 1 mmol/l aspirin was still evident 24 h after drug withdrawal. Sulphinpyrazone also inhibited PGI2 synthesis, but was about 100 fold less potent than aspirin, and the effect of the drug was lost within 24 h of its addition, even when endothelial cells were left in contact with the drug during this period.

Aspirin↗
PubMed1978

Interaction of leukocytes with vascular cells in culture.

The nature, kinetics and cofactor requirements of leukocyte adhesion to cultured vascular cells have been investigated in vitro, using a model system in which leukocyte suspensions are in continuous motion over the cultured cells. Adhesion is assessed by histological examination or by using 51Cr-labelled leukocytes. Leukocytes adhere preferentially to endothelial cell monolayers rather than to smooth muscle cells, adventitial fibroblasts or serum-coated glass. Arterial and venous endothelium are equally good substrates for leukocyte adhesion, and lymphocytes and granulocytes at the same suspension density adhere to endothelial cells in similar numbers. Adherence is greatest during the first 10 min, and is inversely related to flow rate. Numbers of leukocytes adhering to the cell monolayer are proportional to the initial concentration of leukocytes in suspension, although only 2--10% of the leukocytes adhere. Leukocytes that have adhered to the cell monolayer spread over the cells and then migrate, apparently through intercellular junctions. Adhesion requires Ca2+ or Mg2+ ions, but not plasma protein cofactors. Fewer leukocytes adhere to endothelial cells grown for 48 h in rapidly stirred medium than to cells grown under conventional, static conditions.

Blood Vessels↗
PubMed1976

Regional lung function in ankylosing spondylitis.

Xenon-133 was used to study regional pulmonary function in nine patients with chest cage rigidity due to ankylosing spondylitis. In comparison with normal subjects, the patients showed an overall diminution in lung volume and the proportion of inhaled xenon reaching the lung apices was reduced but the distribution of injected xenon was normal. The possible relationship between these findings and apical lung disease in ankylosing spondylitis is mentioned.

Adult↗