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PPARγ-agonist rosiglitazone increases number and migratory activity of cultured endothelial progenitor cells

Endothelial progenitor cells (EPC) are involved in the process of endothelial maintenance and angiogenesis and might be related to endothelial function. EPC function was shown to be impaired in type 2 diabetic patients. Since endothelial dysfunction of type 2 diabetic patients can be ameliorated by...

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Bibliographic Details
Published in:Atherosclerosis 2005-11, Vol.183 (1), p.163-167
Main Authors: Pistrosch, Frank, Herbrig, Kay, Oelschlaegel, Uta, Richter, Susannne, Passauer, Jens, Fischer, Sabine, Gross, Peter
Format: Article
Language:English
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Summary:Endothelial progenitor cells (EPC) are involved in the process of endothelial maintenance and angiogenesis and might be related to endothelial function. EPC function was shown to be impaired in type 2 diabetic patients. Since endothelial dysfunction of type 2 diabetic patients can be ameliorated by treatment with thiazolidinediones we asked whether this treatment might also influence number and function of EPC. We investigated 10 recently diagnosed type 2 diabetic patients and 10 age and sex matched healthy control subjects. After baseline examination of metabolic parameters and EPC, patients received 4 mg rosiglitazone b.i.d. for 12 weeks. We measured EPC number and migratory activity after 3 and 12 weeks of treatment. Migratory activity of EPCs obtained from type 2 diabetic patients at baseline was 40% lower compared to control ( P < 0.05). There was no significant difference of EPC number between patients (323 ± 19) and controls (358 ± 25) at baseline. Treatment of patients with rosiglitazone normalized impaired migratory activity of EPC and increased EPC number (464 ± 33, P < 0.01). In addition treatment improved glycemic control and insulin sensitivity. Twelve-week treatment with rosiglitazone improved EPC number and migratory activity of type 2 diabetic patients. The latter mechanism may contribute to the recently observed improvement of endothelial function by rosiglitazone in type 2 diabetes.
ISSN:0021-9150
1879-1484
DOI:10.1016/j.atherosclerosis.2005.03.039