ArticleInternational journal of clinical and experimental pathology2020
miR-16-5p and miR-145-5p trigger apoptosis in human gingival epithelial cells by down-regulating BACH2.
Article in International journal of clinical and experimental pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Epigenetic factors associated with peri-implantitis: a review.Journal of Zhejiang University. Science. B · 2025Review
- METTL3 mediates CPB1 expression by regulating transcription factor BACH2 to promote apoptosis and oxidative stress of lens epithelial cells.Journal of bioenergetics and biomembranes · 2025Article
- Periodontal Tissue Homoeostasis, Immunity, the Red Complex Pathogens, and Dysbiosis: Unraveling the microRNA Effect.MicroRNA (Shariqah, United Arab Emirates) · 2025Review
- miR-16-5p aggravates sepsis-associated acute kidney injury by inducing apoptosis.Renal failure · 2024Article
- Review
- circ_SPEF2 Regulates the Balance of Treg Cells by Regulating miR-16-5p/BACH2 in Lymphoma and Participates in the Immune Response.Tissue engineering and regenerative medicine · 2023Article
- Gingival Tissue MiRNA Expression Profiling and an Analysis of Periodontitis-Specific Circulating MiRNAs.International journal of molecular sciences · 2023Article
- Comprehensive analysis of miRNAs, lncRNAs and mRNAs profiles in backfat tissue between Daweizi and Yorkshire pigs.Animal bioscience · 2023Article
- Elevated mir-145-5p is associated with skeletal muscle dysfunction and triggers apoptotic cell death in C2C12 myotubes.Journal of muscle research and cell motility · 2022Article
- Crucial Roles of microRNA-16-5p and microRNA-27b-3p in Ameloblast Differentiation Through Regulation of Genes Associated With Amelogenesis Imperfecta.Frontiers in genetics · 2022Article
Corrections and comments
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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
backgroundPeriodontitis is the second most common dental disease worldwide. TNF-α is up-regulated in periodontal disease and induces inflammation and cell apoptosis in gingival epithelial cells (GECs). miRNAs/mRNA axis play an important role in cell progression and inflammation. However, studies on the pathogenesis of periodontitisare still scarce, especially in the regulation mechanism of miRNAs.
methodsThe expression and protein level of miR-16-5p, miR-145-5p, BACH2, and caspase 3 were determined by quantitative real time PCR and western blot, respectively. Cell viability was measured by MTT assay. Cell apoptosis was detected by flow cytometry. Dual-luciferase assay was applied to verify miR-16-5p and miR-145-5p target to the 3'UTR of BACH2.
resultsTNF-α induced miR-16-5p, miR-145-5p and caspase 3 expression, inhibited cell viability, promoted cell apoptosis in GECs. However, down-regulated miR-16-5p and miR-145-5p can restore the effects of TNF-α on GECs. In addition, dual-luciferase assay determined that BACH2 was a common target of miR-16-5p and miR-145-5p. Knockdown of BACH2 induced GECs apoptosis. Of note, cell apoptosis induced by miR-16-5p mimic, miR-145-5p mimic, and TNF-α was significantly reversed by up-regulating BACH2.
conclusionmiR-16-5p and miR-145-5p mediate apoptosis induced by TNF-α in human gingival epithelial cells by targeting BACH2.
Indexed as
Identifiers
32509061PMC7270702W3033183670What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.