ArticleOxidative medicine and cellular longevity2016
Nr2e1 Deficiency Augments Palmitate-Induced Oxidative Stress in Beta Cells.
Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- Article
- NEUROD1 reinforces endocrine cell fate acquisition in pancreatic development.Nature communications · 2023Article
- Sigma‑1 receptor overexpression promotes proliferation and ameliorates cell apoptosis in β‑cells.Molecular medicine reports · 2022Article
- Genetic variation of macronutrient tolerance in Drosophila melanogaster.Nature communications · 2022Article
- Influence of circulating nesfatin-1, GSH and SOD on insulin secretion in the development of T2DM.Frontiers in public health · 2022Article
- TLX, an Orphan Nuclear Receptor With Emerging Roles in Physiology and Disease.Endocrinology · 2021Review
- Sigma receptor knockdown augments dysfunction and apoptosis of beta cells induced by palmitate.Experimental biology and medicine (Maywood, N.J.) · 2021Article
- Computer-Aided Discovery of Small Molecule Inhibitors of Transcriptional Activity of TLX (NR2E1) Nuclear Receptor.Molecules (Basel, Switzerland) · 2018Article
- Oxidative Stress in Pancreatic Beta Cell Regeneration.Oxidative medicine and cellular longevity · 2017Review
- Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear receptor subfamily 2 group E member 1 (Nr2e1) has been regarded as an essential regulator of the growth of neural stem cells. However, its function elsewhere is unknown. In the present study, we generated Nr2e1 knockdown MIN6 cells and studied whether Nr2e1 knockdown affected basal beta cell functions such as proliferation, cell death, and insulin secretion. We showed that knockdown of Nr2e1 in MIN6 cells resulted in increased sensitivity to lipotoxicity, decreased proliferation, a partial G0/G1 cell-cycle arrest, and higher rates of apoptosis. Moreover, Nr2e1 deficiency exaggerates palmitate-induced impairment in insulin secretion. At the molecular level, Nr2e1 deficiency augments palmitate-induced oxidative stress. Nr2e1 deficiency also resulted in decreases in antioxidant enzymes and expression level of Nrf2. Together, this study indicated a potential protective effect of Nr2e1 on beta cells, which may serve as a target for the development of novel therapies for diabetes.
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Registered trials
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