Altered cellular signalling and decreased platelet sensitivity to adenosine in insulin-dependent diabetic patients with proliferative retinopathy
| Autor: | E. D. Saggerson, M.B. Cooper, D.J. Betteridge, K.C.B. Tan, J.A. Gasser |
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| Rok vydání: | 1993 |
| Předmět: |
Blood Platelets
medicine.medical_specialty Adenosine Platelet Aggregation Prostaglandin Adenosine-5'-(N-ethylcarboxamide) Adenylyl cyclase chemistry.chemical_compound GTP-Binding Proteins Diabetes mellitus Internal medicine medicine Humans Platelet Forskolin Binding Sites Diabetic Retinopathy Cell Membrane Colforsin Receptors Purinergic Cell Biology Middle Aged medicine.disease Adenosine receptor Epoprostenol Adenosine Diphosphate Adenosine diphosphate Endocrinology Diabetes Mellitus Type 1 chemistry Female medicine.drug Signal Transduction |
| Zdroj: | Cellular signalling. 5(2) |
| ISSN: | 0898-6568 |
| Popis: | Platelets from patients with insulin-dependent diabetes with proliferative retinopathy showed the same reactivity to ADP as those from control subjects. Responsiveness of platelets to the aggregation inhibitor adenosine and to the analogue N-ethylcarboxamidoadenosine was decreased in diabetes. In contrast, responsiveness to the anti-aggregatory effects of prostaglandin I2 was not significantly altered in diabetes. Platelets from diabetic patients exhibited decreased formation of cyclic AMP in response to N-ethylcarboxamidoadenosine compared with those from control subjects. In contrast, when adenylyl cyclase was stimulated by prostaglandin I2 or by forskolin, no differences in cyclic AMP formation were observed between control and diabetic platelets. Diabetes was associated with an apparent loss of high-affinity binding of [3H]N-ethylcarboxamidoadenosine to platelet membranes. Possible mechanisms that could contribute to this diabetes-induced change in signalling through the platelet A2 adenosine receptor are discussed. |
| Databáze: | OpenAIRE |
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