ArticleExperimental and therapeutic medicine2019
MicroRNA-18 promotes apoptosis of islet β-cells via targeting NAV1.
Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- PBMCs to Stress-Associated miR-18a-5p and miR-22-3p Ratios as New Indicators of Metabolic Syndrome.BioMed research international · 2020Trial
- Comprehensive analysis of the relationship between RNA modification writers and immune microenvironment in head and neck squamous cell carcinoma.BMC immunology · 2024Article
- The Parasite-Derived Peptide, FhHDM-1, Selectively Modulates miRNA Expression inJournal of diabetes research · 2024Article
- Holistic expression of miR-17-92 cluster in obesity, kidney diseases, cardiovascular diseases, and diabetes.Molecular biology reports · 2023Review
- Targeting the PI3K/Akt signaling pathway in pancreatic β-cells to enhance their survival and function: An emerging therapeutic strategy for type 1 diabetes.Journal of diabetes · 2022Review
- Article
- ENPP4 overexpression is associated with no recovery from Barrett's esophagus.International journal of clinical and experimental pathology · 2020Article
- MicroRNA-448 modulates the progression of neuropathic pain by targeting sirtuin 1.Experimental and therapeutic medicine · 2019Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The detailed pathogenesis of diabetes mellitus (DM) remains to be fully elucidated. The purpose of the present study was to explore the role of microRNA (miR)-18 in DM and its underlying mechanisms, providing novel ideas for the treatment of the disease. After inflammatory factor-mediated induction, miR-18 expression in the islet β-cell line MIN6 was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). miR-18 mimics and miR-18 inhibitor were then constructed and transfected into MIN6 cells. The mRNA levels of pro-insulin in MIN6 cells were also detected by RT-qPCR. Released insulin levels and insulin secretion function of MIN6 cells were accessed by ELISA and glucose-stimulated insulin secretion assay, respectively. Apoptosis of MIN6 cells was detected by a terminal deoxynucleotidyl transferase-mediated deoxyuridinetriphosphate nick end labeling assay and western blot analysis of apoptotic proteins. The binding interaction of miR-18 and neuron navigator 1(NAV1), a constituent of the phosphoinositide 3-kinase (PI3K)/AKT pathway, was assessed using a dual-luciferase reporter gene assay. Finally, the regulatory effect of miR-18 on the PI3K/AKT pathway was determined by western blot analysis. After induction of inflammatory factors in MIN6 cells, miR-18 expression was markedly upregulated. Transfection with miR-18 mimics inhibited pro-insulin levels, as well as insulin production and secretion capacity. miR-18 knockdown partially abrogated the inhibited insulin secretion capacity induced by interleukin-1β (IL-1β) treatment. In addition, apoptosis of MIN6 cells was increased by miR-18 mimics. The dual-luciferase reporter gene assay confirmed the direct binding of miR-18 to NAV1. Western blot analysis suggested that miR-18 markedly inhibited the PI3K/AKT pathway in MIN6 cells. In conclusion, miR-18 expression is upregulated by IL-1β induction in islet β-cells. It was demonstrated that miR-18 promotes apoptosis of islet β-cells at least partially by inhibiting NAV1 expression and insulin production via suppression of the PI3K/AKT pathway.
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