ArticleJournal of molecular neuroscience : MN2016
Inhibition of Ectodermal-Neural Cortex 1 Protects Neural Cells from Apoptosis Induced by Hypoxia and Hypoglycemia.
Article in Journal of molecular neuroscience : MN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Comprehensive pan-cancer analysis reveals ENC1 as a promising prognostic biomarker for tumor microenvironment and therapeutic responses.Scientific reports · 2024Article
- The concept of resilience to Alzheimer's Disease: current definitions and cellular and molecular mechanisms.Molecular neurodegeneration · 2024Review
- miR-18a-5p shuttled by mesenchymal stem cell-derived extracellular vesicles alleviates early brain injury following subarachnoid hemorrhage through blockade of the ENC1/p62 axis.Cell and tissue research · 2023Article
- Expression and clinical significance ofJournal of gastrointestinal oncology · 2023Article
- Long Non-coding RNA MIAT Knockdown Prevents the Formation of Intracranial Aneurysm by Downregulating ENC1 via MYC.Frontiers in physiology · 2020Article
- Identification of genes associated with dissociation of cognitive performance and neuropathological burden: Multistep analysis of genetic, epigenetic, and transcriptional data.PLoS medicine · 2017Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ectodermal-neural cortex 1 (Enc1), a member of the KELCH family, is widely expressed in the nervous system and plays an important role in nervous system development. However, the function of Enc1 in neural survival following apoptosis induced by hypoxia and hypoglycemia remains unclear. In this study, we aimed to investigate the role of Enc1 in the cell survival of neurons subjected to apoptosis induced by oxygen-glucose deprivation (OGD) and the potential underlying mechanism. The in vitro cell model of neuron OGD was established by anoxia/hypoglycemic injury. Real-time quantitative PCR and Western blot analyses showed that Enc1 was significantly reduced in neurons under anoxia/hypoglycemic injury. Knockdown of Enc1 by small interfering RNA markedly promoted the survival of neurons under anoxia/hypoglycemia. Moreover, knockdown of Enc1 inhibited neuronal apoptosis. Conversely, overexpression of Enc1 showed the opposite effect. Further, data demonstrated that Enc1 might regulate neuron survival through heme oxygenase-1 (HO-1) and nuclear factor erythroid 2-related factor (Nrf2). Taken together, our study suggests that knockdown of Enc1 protects newborn neurons from apoptosis induced by OGD associated with Nrf2 and HO-1, providing a novel molecular target for the treatment of neonatal apoptosis induced by hypoxia and hypoglycemia brain injury.
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Registered trials
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