Endothelial Abnormalities in Adolescents with Type 1 Diabetes: A Biomarker for Vascular Sequelae? - 07/03/14
, Aneesh Tosh, MD, MS f, Chandan Saha, PhD b, Myka Estes, BS c, Julie Mund, MS c, Laura E. Mead, BS c, Izlin Lien, MD a, David A. Ingram, MD c, d, Laura S. Haneline, MD c, e
Reprint requests: Dr Linda A. DiMeglio, Pediatric Endocrinology and Diabetology, Room 5960; 702 Barnhill Drive, Indianapolis, IN 46202-5225.Abstract |
Objective |
To evaluate whether counts of circulating colony forming unit-endothelial cells (CFU-ECs), cells co-expressing CD34, CD133, and CD31 (CD34+CD133+CD31+), and CD34+CD45- cells are altered in adolescents with type 1 diabetes and if the changes in counts correlate with endothelial dysfunction.
Study design |
Adolescents with diabetes (ages 18 to 22 years) and race- and sex-matched control subjects were studied. We assessed circulating CFU-ECs, using colony assays, and CD34+CD133+CD31+ and CD34+CD45- cells, using poly-chromatic flow cytometry. CFU-ECs and CD34+CD133+CD31+ are hematopoietic-derived progenitors that inversely correlate with cardiovascular risk in adults. CD34+CD45- cells are enriched for endothelial cells with robust vasculogenic potential. Vascular reactivity was tested by laser Doppler iontophoresis.
Results |
Subjects with diabetes had lower CD34+CD133+CD31+ cells, a trend toward reduced CFU-ECs, and increased CD34+CD45- cells compared with control subjects. Endothelium-dependent vasodilation was impaired in subjects with diabetes, which correlated with reductions in circulating CD34+CD133+CD31+ cells.
Conclusions |
Long-term sequelae of type 1 diabetes include vasculopathies. Endothelial progenitor cells promote vascular health by facilitating endothelial integrity and function. Lower CD34+CD133+CD31+ cells may be a harbinger of future macrovascular disease risk. Higher circulating CD34+CD45- cells may reflect ongoing endothelial damage. These cells are potential biomarkers to guide therapeutic interventions to enhance endothelial function and to prevent progression to overt vascular disease.
Le texte complet de cet article est disponible en PDF.Mots-clés : A1C, CFU-ECs, CPCs, ECFCs, EPCs, hsCRP, MNCs, PU
Plan
| Supported by UL1RR025761Indiana Clinical and Translational Sciences Institute (L.D. and D.I), P30 CA08709 (D.I. and L.H.), and the Riley Children's Foundation (D.I. and L.H.). The authors declare no conflicts of interest. |
Vol 157 - N° 4
P. 540-546 - octobre 2010 Retour au numéro
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