Pharmacological and biochemical characterization of purified A<sub>2a</sub> adenosine receptors in human platelet membranes by [<sup>3</sup>H]‐CGS 21680 binding

Varani, Katia; Gessi, Stefania; Dalpiaz, Alessandro; Borea, Pier Andrea

doi:10.1111/j.1476-5381.1996.tb15341.x

Cited by 88 publications

(57 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…26,27 Reperfusion induces a vigorous inflammatory response and a dramatic increase in neutrophil adherence to the reperfused endothelium, which leads to capillary plugging, edema, and a reduction in coronary blood flow. 26 A 2A ARs are widely expressed on blood-borne cells (including T lymphocytes, monocytes, neutrophils, and platelets 7,8,28,29 ). Stimulation of A 2A ARs on bone marrow-derived cells mediates immunosuppression 28 and inhibits neutrophil oxidative activity by a Gs protein-cAMP-dependent pathway.…”

Section: Discussionmentioning

confidence: 99%

Infarct-Sparing Effect of A _2A -Adenosine Receptor Activation Is Due Primarily to Its Action on Lymphocytes

et al. 2005

View full text Add to dashboard Cite

Background-A 2A -adenosine receptor (A 2A AR) activation on reperfusion after ischemia reduces the size of myocardial infarction, but the mechanism of action has not been fully defined. Methods and Results-We created chimeric mice by bone marrow transplantation from A 2A AR-knockout or green fluorescent donor mice to irradiated congenic C57BL/6 (B6) recipients. In the GFP chimeras, we were unable to detect green fluorescent-producing cells in the vascular endothelium, indicating that bone marrow-derived cells were not recruited to endothelium at appreciable levels after bone marrow transplantation and/or acute myocardial infarction. Injection of 5 or 10 g/kg of a potent and selective agonist of A 2A AR, ATL146e, had no effect on hemodynamic parameters but reduced infarct size in B6 mice after 45 minutes of left anterior descending artery occlusion followed by 24 hours of reperfusion to 42.

show abstract

Section: Discussionmentioning

confidence: 99%

Infarct-Sparing Effect of A _2A -Adenosine Receptor Activation Is Due Primarily to Its Action on Lymphocytes

et al. 2005

View full text Add to dashboard Cite

show abstract

“…This connection between LXR and StAR, introduced in this issue of the JCI by Cummins et al (5), provides a new avenue for regulation of steroid synthesis. This may extend to other steroidogenic processes, including testosterone synthesis in the Leydig cells of the testis, estrogens in the ovary, and even neurosteroids produced in glial cells of the brain, each of which utilize StAR.…”

mentioning

confidence: 99%

New insights into the regulation of inflammation by adenosine

Linden

2006

Journal of Clinical Investigation

View full text Add to dashboard Cite

“…Adenosine is known to modulate platelet function via adenosine A 2 receptors (36). The dose of CGS21680C used in the present study was specific for the adenosine A 2 receptors (21,22). Since we demonstrated that adenosine and CGS21680C, not CHA, an adenosine A 1 agonist, reduced the expression of P-selectin and neutrophil-platelet adhesion, effects of adenosine occur mainly via adenosine A 2 receptors.…”

Section: Discussionmentioning

confidence: 99%

“…The doses of CHA and CGS21680C used in this study selectively stimulate adenosine A 1 and A 2 receptors, respectively (21,22). The percentage of platelets that expressed P-selectin in PRP and of neutrophils that bound to platelets in erythrocyte-lysed blood were determined by flow cytometric analysis.…”

Section: Study Protocols Protocol 1 Effects Of Blockade Of Adenosinementioning

confidence: 99%

Endogenous adenosine inhibits P-selectin-dependent formation of coronary thromboemboli during hypoperfusion in dogs.

Minamino¹,

Kitakaze²,

Asanuma³

et al. 1998

J. Clin. Invest.

View full text Add to dashboard Cite

The activation of platelets and the formation of neutrophilplatelet conjugates may lead to the development of thromboemboli. We studied whether blockade of adenosine receptors during coronary hypoperfusion may cause thromboemboli via P-selectin-dependent mechanisms in 30 open-chest dogs. When coronary blood flow was reduced to 20% of the control, it was stable at low levels with increases in adenosine levels. When 8-p -sulfophenyltheophylline, an adenosine receptor antagonist, was infused during coronary hypoperfusion, coronary blood flow decreased gradually and approached almost zero 20 min after its administration. Histological examination revealed thromboemboli in the small coronary vessels. During hypoperfusion in the presence of 8-p -sulfophenyltheophylline, the mAb against P-selectin attenuated both the reduction in coronary blood flow and the formation of thromboemboli, and improved contractile and metabolic dysfunction of the myocardium. Flow cytometric analysis indicated that the expression of P-selectin on platelet and neutrophil-platelet adhesion were increased during coronary hypoperfusion, and that both were further augmented by 8-p -sulfophenyltheophylline. Immunohistochemical examination showed no staining of P-selectin in the ischemic myocardium. Adenosine inhibited the thrombininduced expression of P-selectin on platelet and neutrophilplatelet adhesion via adenosine A 2 receptors. Adenosine appears to inhibit the formation of thromboemboli during coronary hypoperfusion by suppressing the expression of P-selectin on platelets and neutrophil-platelet adhesion. ( J.

show abstract

Pharmacological and biochemical characterization of purified A_2a adenosine receptors in human platelet membranes by [³H]‐CGS 21680 binding

Cited by 88 publications

References 36 publications

Infarct-Sparing Effect of A _2A -Adenosine Receptor Activation Is Due Primarily to Its Action on Lymphocytes

Infarct-Sparing Effect of A _2A -Adenosine Receptor Activation Is Due Primarily to Its Action on Lymphocytes

New insights into the regulation of inflammation by adenosine

Endogenous adenosine inhibits P-selectin-dependent formation of coronary thromboemboli during hypoperfusion in dogs.

Contact Info

Product

Resources

About

Pharmacological and biochemical characterization of purified A2a adenosine receptors in human platelet membranes by [3H]‐CGS 21680 binding

Cited by 88 publications

References 36 publications

Infarct-Sparing Effect of A 2A -Adenosine Receptor Activation Is Due Primarily to Its Action on Lymphocytes

Infarct-Sparing Effect of A 2A -Adenosine Receptor Activation Is Due Primarily to Its Action on Lymphocytes

New insights into the regulation of inflammation by adenosine

Endogenous adenosine inhibits P-selectin-dependent formation of coronary thromboemboli during hypoperfusion in dogs.

Contact Info

Product

Resources

About

Pharmacological and biochemical characterization of purified A_2a adenosine receptors in human platelet membranes by [³H]‐CGS 21680 binding

Infarct-Sparing Effect of A _2A -Adenosine Receptor Activation Is Due Primarily to Its Action on Lymphocytes

Infarct-Sparing Effect of A _2A -Adenosine Receptor Activation Is Due Primarily to Its Action on Lymphocytes