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Biochem Biophys Res Commun. 2009 Mar 27;381(1):81-3. doi: 10.1016/j.bbrc.2009.02.013. Epub 2009 Feb 10.

MicroRNA-221 regulates high glucose-induced endothelial dysfunction.

Author information

  • 1Texas Heart Institute and The University of Texas Medical School, Heart Failure and Stem Cell, P.O. Box 20345, MC 2-255, 6770 Bertner Avenue, Houston, TX 77030, USA. Yangxin_li@yahoo.com

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.

PMID:
19351599
[PubMed - indexed for MEDLINE]
PMCID:
PMC2670889
Free PMC Article

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