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Vol 17, No 1 (2011)
Research paper
Published online: 2011-04-22

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RAGE and ADAM17 genes expression in peripheral blood monocytes in patients with type 2 diabetes. Implications of rosiglitazone therapy

Małgorzata Gacka, Anna Sadakierska-Chudy, Tadeusz Dobosz, Stanisław Szymaniec, Dorota Bednarska-Chabowska, Rajmund Adamiec
Acta Angiologica 2011;17(1):98-108.

Abstract

Background. Diabetes is a metabolic disease which predisposes to serious cardiovascular disorders. Peripheral blood monocytes play a major role in the setting of hyperglycaemia and insulin resistance, when they undergo activation and stimulate atherosclerosis. The aim of the study was to assess the expression of RAGE (receptor of advanced glycation end products) and ADAM17 (a disintegrin and metalloproteinase 17) genes in peripheral blood monocytes in patients with type 2 diabetes during rosiglitazone therapy.
Material and methods. Monocytes were isolated from peripheral blood samples taken before and after 22 weeks of rosiglitazone therapy, from 45 patients with type 2 diabetes. Expression of RAGE and ADAM17 genes was assessed with RT-PCR (ABI Prism 7900HT Sequence Detection System). Gene expression in the study group was determined in comparison with patterns obtained from 22 healthy volunteers. Others tests were conducted by means of routine lab assays.
Results. ADAM17 gene expression was detected in 78% of patients and RAGE gene in 71% in the study group as compared to control group. Rosiglitazone therapy did not result in a significant change in both genes’ expression (log RQ for ADAM17 before treatment 1.34 ± 1.11 vs. after treatment 1.20 ± 0.94; p = 0.464, and log RQ for RAGE 0.986 ± 1.02 vs. 1.17 ± 0.96; p = 0.675). Significant HbA1c reduction was observed after rosiglitazone therapy (before treatment 7.32 ± 1.76% vs. after treatment 6.69 ± 1.02%; p = 0.039).
Conclusions. Rosiglitazone therapy and improved glycaemic control in type 2 diabetes does not influence expression of ADAM17 and RAGE genes in peripheral blood monocytes.
Acta Angiol 2011; 17, 1: 98–108

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