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Silencing of long non-coding antisense RNA brain-derived neurotrophic factor attenuates hypoxia/ischemia-induced neonatal brain injury
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Silencing of long non-coding antisense RNA brain-derived neurotrophic factor attenuates hypoxia/ischemia-induced neonatal brain injury
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Silencing of long non-coding antisense RNA brain-derived neurotrophic factor attenuates hypoxia/ischemia-induced neonatal brain injury
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Journal Article
Silencing of long non-coding antisense RNA brain-derived neurotrophic factor attenuates hypoxia/ischemia-induced neonatal brain injury
2020
Overview
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. Reverse transcription-quantitative PCR (RT-qPCR) assays indicated that BDNF-AS expression was significantly upregulated in HI-injured neonatal brains and hippocampal neurons. However, BDNF expression was downregulated in HI-injured neonatal brains and hippocampal neurons. Cell Counting Kit-8 assays, Hoechst staining, calcein-AM/PI staining, immunostaining, water maze tests and rotarod tests demonstrated that BDNF-AS silencing protected against hypoxia-induced primary hippocampal neuron injury in vitro and HI-induced brain injury in vivo. Mechanistically, RT-qPCR assays and western blotting indicated that BDNF-AS silencing led to increased expression of BDNF and activated the BDNF-mediated signaling pathway, as demonstrated by increased expression levels of BDNF, phosphorylated-Akt and phosphorylated-tropomyosin receptor kinase B. Collectively, the present study provides important insights into the pathogenesis of HIBD, and it was indicated that BDNF-AS silencing may be a promising approach for the treatment of neonatal HIBD.
Publisher
D.A. Spandidos,Spandidos Publications,Spandidos Publications UK Ltd
Subject
