microRNA-221 regulates high glucose-induced endothelial dysfunction
- 10 February 2009
- journal article
- research article
- Published by Elsevier BV in Biochemical and Biophysical Research Communications
- Vol. 381 (1), 81-83
- https://doi.org/10.1016/j.bbrc.2009.02.013
Abstract
Persistent hyperglycemia in diabetes causes endothelial cell dysfunction. Exposure to high levels of glucose, which mimics hyperglycemia, induced expression of microRNA 221 (miR-221) but reduced expression of c-kit, the receptor for stem cell factor in human umbilical vein endothelial cells (HUVECs). In addition, high glucose treatment impaired endothelial cell migration. Incubation with the antisense miR-221 oligonucleotide AMO-221 reduced expression of miR-221 and restored c-kit protein expression in HUVECs treated with high levels of glucose. Furthermore, AMO-221 treatment abolished the inhibitory effect of high glucose exposure on HUVECs transmigration. Thus, under hyperglycemic conditions, miR-221 is induced in HUVECs, which consequently triggers inhibition of c-kit and impairment of HUVECs migration. These findings suggest that manipulation of the miR-221-c-kit pathway may offer a novel strategy for treatment of vascular dysfunction in diabetic patients.Keywords
Funding Information
- American Heart Association (0765149Y)
- Macdonald Stewart Foundation (07RDM008)
- National Institutes of Health (R01HL69509)
- U.S. Department of Defense
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