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Genet Mol Res ; 15(2)2016 May 12.
Artigo em Inglês | MEDLINE | ID: mdl-27323011

RESUMO

Brain damage caused by perinatal asphyxia is dangerous for neonatal infants, but the mechanism by which it occurs remains elusive. In this study, microRNA-152 (miR-152) expression was induced by low oxygen levels in rat models of hypoxia brain damage, as well as in human brain microvascular endothelial cells (HBMECs) cultured in vitro. Analysis of the sequence of miR-152 revealed that the phosphatase and tensin homolog gene (PTEN) is probably the target of miR-152 both in humans and rats. When HBMECs were transfected with miR-152 mimics, PTEN expression was inhibited at both the mRNA and protein levels. Moreover, transfection with the miR-152 mimic also inhibited apoptosis induced by hypoxia. Furthermore, expression of the pro-apoptotic gene Bax was downregulated while the anti-apoptotic gene Bcl2 was upregulated after miR-152 mimic transfection. Taken together, these results indicate that miR-152 induced by hypoxia suppresses cell apoptosis and acts as a protective factor during hypoxia by repressing PTEN.


Assuntos
Células Endoteliais/enzimologia , Hipóxia Encefálica/metabolismo , MicroRNAs/biossíntese , Oxigênio/metabolismo , PTEN Fosfo-Hidrolase/genética , Animais , Apoptose/genética , Encéfalo/irrigação sanguínea , Hipóxia Celular/fisiologia , Células Endoteliais/metabolismo , Células HEK293 , Humanos , Hipóxia Encefálica/patologia , Masculino , Microvasos/enzimologia , Microvasos/metabolismo , Modelos Animais , PTEN Fosfo-Hidrolase/metabolismo , Ratos , Ratos Sprague-Dawley
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