Long non-coding RNA Snhg3 protects against hypoxia/ischemia-induced neonatal brain injury.
Exp Mol Pathol
; 112: 104343, 2020 02.
Article
de En
| MEDLINE
| ID: mdl-31751562
ABSTRACT
Hypoxic-ischemic brain damage (HIBD) is a major cause of morbidity and mortality in the preterm and term infant. However, the precise mechanism of HIBD remains largely elusive. As a newly discovered long non-coding RNA, small nucleolar RNA host gene 3 (Snhg3) has shown its important roles in cell apoptosis, proliferation, and disease development. In this study, we determined the role of Snhg3 in the pathogenesis of HIBD. Snhg3 expression was significantly down-regulated in the neonatal brain and primary hippocampal cells response to hypoxic/ischemic stress. Snhg3 overexpression protected against hypoxic/ischemic-induced brain injury in vivo and hippocampal cell injury in vitro. Snhg3 acted as the sponge of miR-196 in the hippocampal cells by regulating the expression of miR-196 target genes, XIAP and CAAP1. Moreover, Snhg3 overexpression decreased brain infarct size and ameliorated hypoxic-ischemic neonatal brain damage. This study suggests that Snhg3 is a potential target for the treatment of HIBD.
Mots clés
Texte intégral:
1
Collection:
01-internacional
Base de données:
MEDLINE
Sujet principal:
Lésions encéphaliques
/
Hypoxie-ischémie du cerveau
/
MicroARN
/
ARN long non codant
Type d'étude:
Prognostic_studies
Limites:
Animals
/
Humans
/
Male
Langue:
En
Journal:
Exp Mol Pathol
Année:
2020
Type de document:
Article
Pays d'affiliation:
Chine