Silencing of long non‑coding antisense RNA brain‑derived neurotrophic factor attenuates hypoxia/ischemia‑induced neonatal brain injury.

Hypoxic/ischemic (HI) brain damage (HIBD) is a major cause of acute neonatal brain injury, leading to high mortality and serious neurological deficits. The antisense RNA of brain‑derived neurotrophic factor (BDNF‑AS) is transcribed from the opposite strand of the BDNF gene. The aim of the present study was to investigate the role of BDNF‑AS in HI‑induced neuronal cell injury in vivo and in vitro.

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

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.

High-throughput sequencing analysis of lncRNAs in hippocampus tissues with hypoxic-ischemic brain damage.

LncRNAs abundantly expressed in the brain have vital and wide-ranging functions in different biological processes. However, little is currently known regarding the influence of lncRNAs in developing brains after hypoxic-ischemic brain damage (HIBD). In this study, to investigate the lncRNAs expression signatures and the co-expression network of lncRNAs and mRNAs in the brain after HIBD, we established a and detected the expression profiles of lncRNAs in the HIBD brain and a sham control using high-throughput sequencing.

GAS5 silencing protects against hypoxia/ischemia-induced neonatal brain injury.

Hypoxic/ischemic brain damage (HIBD) leads to high neonatal mortality and severe neurologic morbidity. However, the molecular mechanism of HIBD in the neonatal infant is still elusive. Long non-coding RNAs are shown as important regulators of brain development and many neurological diseases.