Long non-coding RNA Snhg3 protects against hypoxia/ischemia-induced neonatal brain injury.

Exp Mol Pathol 2020 02 18;112:104343. Epub 2019 Nov 18.

Department of Pediatrics, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China. Electronic address:

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.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.yexmp.2019.104343DOI Listing
February 2020

Publication Analysis

Top Keywords

neonatal brain
12
snhg3 overexpression
8
brain injury
8
hippocampal cells
8
snhg3
8
long non-coding
8
non-coding rna
8
brain damage
8
brain
6
stress snhg3
4
cells response
4
response hypoxic/ischemic
4
hypoxic/ischemic stress
4
overexpression protected
4
hippocampal cell
4
cell injury
4
vivo hippocampal
4
injury vivo
4
protected hypoxic/ischemic-induced
4
hypoxic/ischemic-induced brain
4

Similar Publications