ArticleInternational journal of molecular medicine2020
Silencing of long non‑coding antisense RNA brain‑derived neurotrophic factor attenuates hypoxia/ischemia‑induced neonatal brain injury.
Article in International journal of molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Comprehensive mapping of the signaling events evoked by SARS-CoV-2 variants delta and omicron in human astrocytes.Scientific reports · 2025Article
- hUC-MSC extracellular vesicles protect against hypoxic-ischemic brain injury by promoting NLRP3 ubiquitination.Biomolecules & biomedicine · 2025Article
- Potential Correlation Between Molecular Biomarkers and Oxidative Stress in Traumatic Brain Injury.International journal of molecular sciences · 2025Review
- Cerebral Hypoxia-Induced Molecular Alterations and Their Impact on the Physiology of Neurons and Dendritic Spines: A Comprehensive Review.Cellular and molecular neurobiology · 2024Review
- LncRNAs and CircRNAs as Strategies against Pathological Conditions Caused by a Hypoxic/Anoxic State.Biomolecules · 2023Review
- Associations of BDNF/BDNF-AS SNPs with Depression, Schizophrenia, and Bipolar Disorder.Journal of personalized medicine · 2023Review
- Long Non-Coding RNAs in Hypoxia and Oxidative Stress: Novel Insights Investigating a Piglet Model of Perinatal Asphyxia.Biology · 2023Article
- Group II Metabotropic Glutamate Receptors Reduce Apoptosis and Regulate BDNF and GDNF Levels in Hypoxic-Ischemic Injury in Neonatal Rats.International journal of molecular sciences · 2022Article
- Neuron-Glia Crosstalk Plays a Major Role in the Neurotoxic Effects of KetamineFrontiers in cell and developmental biology · 2021Article
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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