In vitro vessel-forming capacity of endothelial progenitor cells in high glucose conditions |
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Authors: | Chaiwat?Jiraritthamrong Pakpoom?Kheolamai Yaowalak?U-Pratya Methichit?Chayosumrit Aungkura?Supokawej Sirikul?Manochantr Chairat?Tantrawatpan Hathaitip?Sritanaudomchai Email author" target="_blank">Surapol?IssaragrisilEmail author |
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Institution: | (1) Department of Immunology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, 10700, Thailand;(2) Division of Cell Biology, Department of Pre-clinical Sciences, Faculty of Medicine, Thammasat University, Khlong Luang, Pathumthani, Thailand;(3) Division of Hematology, Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, 10700, Thailand;(4) Siriraj Center of Excellence for Stem Cell Research, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, 10700, Thailand;(5) Department of Clinical Microscopy, Faculty of Medical Technology, Mahidol University, Bangkok, Thailand; |
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Abstract: | In type 2 diabetes, the impairment of vascular repair processes and angiogenesis are due to endothelial progenitor cell (EPC)
dysfunction. In this study, we established a quantitative methodology to assess EPC function by using an in vitro 5-(6)-carboxyfluorescein
diacetate succinimidyl ester-labeling vessel formation assay. The EPCs were cultured in three different glucose concentrations
(100, 189.5, and 295.5 mg/dl of d-glucose) representing normal control and diabetes with either good or poor glycemic control, respectively. We found that
the in vitro vessel-forming capacity was impaired in EPCs cultured in high glucose concentrations compared to normal control
(43.4 ± 0.8% and 34.7 ± 0.7% vs. 50.8 ± 2.1%). We further studied expression of various genes involved in vessel formation.
There was a lower level of angiopoietin 1 gene expression in EPCs cultured in high glucose concentrations. The addition of recombinant angiopoietin 1 significantly
increased the vessel-forming capacity of EPCs cultured in high glucose concentration (35.3 ± 2.0% to 48.8 ± 2.7%), whereas
the addition of angiopoietin 2 (a competitive inhibitor of angiopoietin 1) impaired the vessel-forming capacity of EPCs cultured
in normal glucose concentration (51.8 ± 1.3% to 41.3 ± 0.6%). We conclude that the in vitro vessel-forming capacity of EPCs
cultured in high glucose concentration is impaired due to low levels of angiopoietin 1. |
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