Artigo Acesso aberto Revisado por pares

microRNA-221 regulates high glucose-induced endothelial dysfunction

2009; Elsevier BV; Volume: 381; Issue: 1 Linguagem: Inglês

10.1016/j.bbrc.2009.02.013

ISSN

1090-2104

Autores

Yangxin Li, Yao-Hua Song, Fan Li, Yang Tong, Yao Wei Lu, Yong-Jian Geng,

Tópico(s)

Extracellular vesicles in disease

Resumo

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.

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