ArticleCell death & disease2016
Long non-coding RNA C2dat1 regulates CaMKIIδ expression to promote neuronal survival through the NF-κB signaling pathway following cerebral ischemia.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 110 citations in OpenAlex.
- Integrative multi-omics analysis reveals the drug-protein-ceRNA regulatory network in acute ischemic stroke.Frontiers in molecular biosciences · 2026Article
- The emerging roles of long non-coding RNAs in the nervous system.Nature reviews. Neuroscience · 2025Review
- LncRNA CHRF: molecular mechanisms and therapeutic potentials in cardiovascular diseases, cancers and fibrosis.Frontiers in cell and developmental biology · 2025Review
- Unveiling the role of CaMKII in retinal degeneration: from biological mechanism to therapeutic strategies.Cell & bioscience · 2024Review
- [PI3K/Akt/Erk signaling pathway mediates neuroprotection of CaMKⅡγ and CaMKⅡδ against ischemic reperfusion injury in mice].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Differential expression of non-coding RNAs and association with cerebral ischemic vascular disorders; diagnostic and therapeutic opportunities.Genes & genomics · 2023Review
- Roles of lncRNAs in brain development and pathogenesis: Emerging therapeutic opportunities.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Review
- Association of triglyceride-glucose index with early neurological deterioration events in patients with acute ischemic stroke.Diabetology & metabolic syndrome · 2023Article
- LncRNA BIRF Promotes Brain Ischemic Tolerance Induced By Cerebral Ischemic Preconditioning Through Upregulating GLT-1 via Sponging miR-330-5p.Molecular neurobiology · 2022Article
- Expression and clinical significance of lncRNA BC041954 in ovarian cancer.Experimental and therapeutic medicine · 2022Article
- Effects of ischemic postconditioning and long non-coding RNAs in ischemic stroke.Bioengineered · 2022Review
- Long Non-coding RNAs (lncRNAs), A New Target in Stroke.Cellular and molecular neurobiology · 2022Review
- COMIRESTROKE-A clinical study protocol for monitoring clinical effect and molecular biological readouts ofFrontiers in neurology · 2022Article
- Altered lncRNAs Transcriptomic Profiles in Atherosclerosis-Induced Ischemic Stroke.Cellular and molecular neurobiology · 2022Article
- Role of CaFrontiers in molecular neuroscience · 2022Review
- Long Noncoding RNA SCIRT Promotes HUVEC Angiogenesis via Stabilizing VEGFA mRNA Induced by Hypoxia.Oxidative medicine and cellular longevity · 2022Article
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- Long non-coding RNAs mediate cerebral vascular pathologies after CNS injuries.Neurochemistry international · 2021Review
- New epigenetic players in stroke pathogenesis: From non-coding RNAs to exosomal non-coding RNAs.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Review
1 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Increasing evidence has demonstrated a significant role of long non-coding RNAs (lncRNAs) in diverse biological processes. However, their functions in cerebral ischemia remain largely unknown. Through an lncRNA array analysis in a rat model of focal cerebral ischemia/reperfusion (I/R), we have identified CAMK2D-associated transcript 1 (C2dat1) as a novel I/R-induced lncRNA that regulated the expression of CaMKIIδ in murine models of focal cerebral ischemia. C2dat1 mRNA was upregulated in a time-dependent manner in mouse cortical penumbra after focal ischemic brain injury, which was accompanied by increased expression of CaMKIIδ at transcript and protein levels. The expression patterns of C2dat1 and CAMK2D were confirmed in mouse Neuro-2a cells in response to in vitro ischemia (oxygen-glucose deprivation/reoxygenation, OGD/R). Knockdown of C2dat1 resulted in a significant blockade of CaMKIIδ expression, and potentiated OGD/R-induced cell death. Mechanistically, reduced CaMKIIδ expression upon silencing C2dat1 inhibited OGD/R-induced activation of the NF-κB signaling pathway. Further analysis showed that the downregulation of IKKα and IKKβ expression and phosphorylation, and subsequent inhibition of IκBα degradation accounted for the inhibition of the NF-κB signaling activity caused by silencing C2dat1. In summary, we discovered a novel I/R-induced lncRNA C2dat1 that modulates the expression of CaMKIIδ to impact neuronal survival, and may be a potential target for therapeutic intervention of ischemic brain injury.
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