Identification of a membrane adenosine deaminase binding protein from human placenta

Trotta, Paul P.

doi:10.1021/bi00260a017

Cited by 33 publications

(9 citation statements)

References 44 publications

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“…Subunits thus bound retain catalytic activity (Dadonna and Kelley, 1980). Recent reports indicate that the protein is located on the cell surface and that, under normal conditions, most adenosine deaminase binding sites are unoccupied and therefore able to bind catalytic subunits (Andy and Komfeld, 1982;Trotta, 1982). Accordingly, it is possible that most of the adenosine deaminase retained in the hearts of the animals reported in this study may have been bound to cell surfaces.…”

Section: Discussionmentioning

confidence: 80%

Role of adenosine in the maintenance of coronary vasodilation distal to a severe coronary artery stenosis. Observations in conscious domestic swine.

Gewirtz¹,

Brautigan²,

Olsson³

et al. 1983

Circulation Research

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SUMMARY. The purpose of this study was to test the hypothesis that adenosine is required to maintain arteriolar vasodilation distal to a severe coronary stenosis. Eight closed-chest conscious pigs were prepared by placing a 7.5-mm long stenosis (82% lumenal diameter reduction) in the proximal left anterior descending coronary artery. Regional myocardial blood flow (microsphere technique) was measured at control 1, after 10 minutes of intracoronary infusion of adenosine deaminase (7-10 U/kg per min) distal to the stenosis, and 20-30 minutes after stopping adenosine deaminase infusion. Studies with 125 I-labeled adenosine deaminase were conducted in six additional pigs to document the extent to which infused adenosine deaminase penetrated the interstitial space. I-labeled adenosine deaminase was infused for 10 minutes (10-11 U/kg per min) into the left anterior discending coronary artery. Calculated interstitial fluid concentrations of adenosine deaminase ranged between 71 and 272 U/ml and were at least one order of magnitude greater than that required to deaminate all the adenosine which would be released into the interstitium in response to 15-30 seconds of coronary occlusion. In the primary group of animals (n = 8), endocardial flow (ml/min per g) distal to stenosis at control 1 (1.15 ± 0.33) was reduced vs. endocardial flow in the nonobstructed circumflex zone (1.59 ± 0.38, P < 0.05). Flows in epicardial layers were comparable at control 1 (distal zone = 1.40 ± 0.36 vs. circumflex zone = 1.45 ± 0.41). Distal zone endocardial and epicardial flows did not change vs. control 1 in response to infusion of adenosine deaminase. However, the distakcircumflex epicardial flow ratio declined vs. control 1 (0.98 ± 0.14) during adenosine deaminase infusion (0.87 ± 0.17, P < 0.05). The distakcircumflex endocardial flow ratio during adenosine deaminase (0.72 ± 0.20) was unchanged vs. control 1 (0.76 ± 0.22) but was less than control 2 (0.80 ± 0.18, P < 0.05). Thus, destruction of all or most interstitial adenosine caused only slight relative reduction in regional myocardial blood flow distal to a severe coronary artery stenosis. Accordingly, adenosine contributes only modestly to maintenance of arteriolar vasodilation in this setting or else its absence is almost fully compensated for by another mechanism(s). (Circ Res 53: 42-51, 1983) ADENOSINE is widely regarded as the primary physiological mediator of both reactive hyperemia and autoregulation of the coronary vascular bed (Beme and Rubio, 1979). Although several recent studies (Hester et al., 1982;Jones et al., 1982;Manfredi and Sparks, 1982;Saito et al., 1981) have undertaken tests of the adenosine hypothesis as it applies to reactive hyperemia or autoregulation in response to increased myocardial oxygen demand, none have addressed the role of adenosine in the maintenance of normal or only modestly reduced levels of myocardial blood flow distal to a severe coronary artery stenosis. Accordingly, the present investigation was performed to test the hypothesis that adenos...

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Section: Discussionmentioning

confidence: 80%

Role of adenosine in the maintenance of coronary vasodilation distal to a severe coronary artery stenosis. Observations in conscious domestic swine.

Gewirtz¹,

Brautigan²,

Olsson³

et al. 1983

Circulation Research

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“…10; unpublished observations) have shown that the gp120 molecule detected by mAbS27 and mAbS23 is ADA-BP and that these mAbs identify distinct epitopes on ADA-BP. Past work with polyvalent antibody to ADA-BP has shown its presence in kidney, liver, lung, colon, spleen, and placenta, as well as fibroblasts and leukocytes (12)(13)(14). ADA-BP also occurs in the body fluids such as serum, saliva, and urine.…”

Section: Discussionmentioning

confidence: 99%

Specificity analysis of mouse monoclonal antibodies defining cell surface antigens of human renal cancer.

Finstad¹,

Cordon‐Cardo²,

Bander³

et al. 1985

Proc. Natl. Acad. Sci. U.S.A.

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Six mouse monoclonal antibodies (mAbs) defining separate systems of cell surface antigens of cultured human renal cancer were tested for reactivity with normal fetal and adult tissues and with neoplastic tissues. Five of the mAbs identified glycoproteins of Mr 160,000 (designated S4), Mr Mr 140,000 (F23), Mr 120,000 (S23 and S27), and Mr 115,000 (S22). The glycoprotein component of Mr 120,000 has been shown recently to be the adenosine deaminase binding protein (ADA-BP) and mAbS23 and mAbS27 define two distinct epitopes on ADA-BP. S22 was not detected on any normal fetal or adult tissues but was found on a subset of renal cancers. S4, F23, S23, and S27 defined distinct domains of the nephron: glomerulus (S4), proximal tubules (S4, F23, S23, and S27), and portions of Henle's loop (S23 and S27). mAbS4 also reacted with the interstitial matrix in the renal medulla and of other tissues, and mAbF23 reacted with fetal and adult fibroblasts. The S23 epitope of ADA-BP was expressed by placental trophoblasts and epithelial cells of breast, prostate, lung, and colon, whereas the S27 epitope was detected on a more limited range of cell types (trophoblasts and prostate epithelium). A panel of 20 renal cell carcinomas was typed for expression of these antigens; 7 phenotypes could be distinguished, with the S4+/F23+/S23+/S27+/S22+ or - phenotype (15 cases) being most common. The other antigenic system, V1, identified a heat-stable antigen that was widely expressed on cultured cell types but showed a restricted pattern of reactivity in tissues. V1 expression was limited to the adrenal cortex, Leydig cells, and the theca of ovarian follicles, and to adrenal cortical carcinomas.

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“…This hypothesis is supported by the markedly reduced tritium retention when perfusates contained 100 /SM-adenosine (Table 1). It has been reported that an adenosine deaminase-binding protein is associated with the human microvillous trophoblast membrane (Trotta, 1982). If a similar situation exists in guinea-pig placenta a fraction of the inosine produced during passage through the uterine circulation (Fig.…”

Section: Adenosine Metabolismmentioning

confidence: 82%

Transport and metabolism of adenosine in the perfused guinea‐pig placenta.

Wheeler

Yudilevich

1988

The Journal of Physiology

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SUMMARY1. Uptake and metabolism of adenosine were investigated from both maternal (M) and fetal (F) circulations of the isolated, dually perfused guinea-pig placenta by using a single-circulation paired-tracer ([14C]sucrose as extracellular reference, and [3H]adenosine) dilution technique.2. Maximal [3H]adenosine uptakes (percentage of dose) from adenosine-free perfusates were 75+1 and 87+2% (mean+S.E. of mean) at maternal and fetal blood-tissue interfaces respectively. Rapid backflux (percentage of influx) of tritium (labelled adenosine and/or adenosine derivatives) from the placental tissue into the ipsilateral circulation was higher at the fetal (24 + 2 %) than at the maternal side (11+2%).3. Tritium uptakes were reduced to 50 + 4 (M) and 60 + 6 % (F) when the perfusion medium contained 100 ,IM-unlabelled adenosine; backflux was highly stimulated (44 % M and 84 % F). Neither uptake nor backflux were affected by inosine, uridine, adenine or hypoxanthine present in the perfusion medium (1 mM).4. Tissue sequestration of tritium (5-6 min) was approximately 60% of the injected dose when perfusates were adenosine-free and 20 % or less in the presence of 100 /IM-adenosine. 9. The present data demonstrate DIP-and NBMPR-sensitive carrier-mediated adenosine uptake at the brush-border side of the syncytiotrophoblast (maternalfacing) and at the fetal side. In the latter case the role of the basal syncytial membrane and the fetal endothelium could not be distinguished. Rapid metabolism of adenosine also occurs at both blood-tissue interfaces. The placenta may therefore be involved in the regulation of adenosine-related functions in mother and fetus during pregnancy.

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Identification of a membrane adenosine deaminase binding protein from human placenta

Cited by 33 publications

References 44 publications

Role of adenosine in the maintenance of coronary vasodilation distal to a severe coronary artery stenosis. Observations in conscious domestic swine.

Role of adenosine in the maintenance of coronary vasodilation distal to a severe coronary artery stenosis. Observations in conscious domestic swine.

Specificity analysis of mouse monoclonal antibodies defining cell surface antigens of human renal cancer.

Transport and metabolism of adenosine in the perfused guinea‐pig placenta.

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