ArticleAmerican journal of translational research2019
MicroRNA-495 enhances chondrocyte apoptosis, senescence and promotes the progression of osteoarthritis by targeting AKT1.
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Network Pharmacology and Experimental Evidence Indicate That Dihydrochelerythrine fromJournal of inflammation research · 2026Article
- LncRNA PTS-1 Protects Against Osteoarthritis Through the miR-8085/E2F2 Axis.Journal of inflammation research · 2025Article
- miR-495 promotes intestinal epithelial cell apoptosis through downregulation of Sphingosine-1-phosphate.Physiological reports · 2024Article
- Inflammatory and Metabolic Signaling Interfaces of the Hypertrophic and Senescent Chondrocyte Phenotypes Associated with Osteoarthritis.International journal of molecular sciences · 2023Review
- STAT3 expression in patients with fragility fractures and its effect on the biological function of osteoblasts.Cell and tissue banking · 2023Article
- Autophagy and apoptosis: regulatory factors of chondrocyte phenotype transition in osteoarthritis.Human cell · 2023Review
- Flavokawain A alleviates the progression of mouse osteoarthritis: AnFrontiers in bioengineering and biotechnology · 2022Article
- A Network Pharmacology-Based Study of Potential Targets of Angelicae Pubescentis-Herba Taxilli Compound for the Treatment of Osteoarthritis.Computational and mathematical methods in medicine · 2022Article
- Downregulation of MicroRNA-495 Alleviates IL-1β Responses among Chondrocytes by Preventing SOX9 Reduction.Yonsei medical journal · 2021Article
- Review
- miR-205 and HMGB1 expressions in chronic periodontitis patients and their associations with the inflammatory factors.American journal of translational research · 2021Article
- CircSNHG5 Sponges Mir-495-3p and Modulates CITED2 to Protect Cartilage Endplate From Degradation.Frontiers in cell and developmental biology · 2021Article
- Engineered-extracellular vesicles as an optimistic tool for microRNA delivery for osteoarthritis treatment.Cellular and molecular life sciences : CMLS · 2021Review
- CircSERPINE2 weakens IL-1β-caused apoptosis and extracellular matrix degradation of chondrocytes by regulating miR-495/TGFBR2 axis.Bioscience reports · 2020Article
- Pathogenesis of Osteoarthritis: Risk Factors, Regulatory Pathways in Chondrocytes, and Experimental Models.Biology · 2020Review
- Exosomal miRNAs in osteoarthritis.Molecular biology reports · 2020Review
- [Expression of microRNA-495-5p in preterm infants with bronchopulmonary dysplasia: a bioinformatics analysis].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2020Article
- Non-Coding RNAs in Cartilage Development: An Updated Review.International journal of molecular sciences · 2019Review
- Exploration of the mechanism of tetramethoxyflavone in treating osteoarthritis based on network pharmacology and molecular docking.Tzu chi medical journalArticle
- MicroRNAs as Key Regulators of Degeneration and Inflammation in Osteoarthritis: A Narrative Review.Saudi journal of medicine & medical sciencesReview
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is a common multifactorial degenerative articular disease among the aging population. The current investigation aimed to elucidate the function of microRNA-495 (miR-495) in the development of OA. We found that miR-495 was upregulated in the cartilage of OA patients. Transfection of a miR-495 mimic into rat primary chondrocytes, human chondrocytes (HC) and SW1353 chondrosarcoma cells inhibited AKT1 expression, proliferation and scratch wound closure and induced apoptosis. Transfection of a miR-495 inhibitor produced an opposite effect. Furthermore, the production of cartilage degeneration-related substances was modified by miR-495. Luciferase reporter gene assay revealed that AKT1 is directly repressed by miR-495. Moreover, the levels of AKT1, p-S6 and p-mTOR diminished in chondrocytes overexpressing miR-495. AKT1 overexpression amplified p-S6 and p-mTOR levels as well as abolished miR-495 mimic-induced apoptosis and inhibition of proliferation. In the surgically induced rat OA model, apoptosis of chondrocytes and cartilage degeneration were remedied by the administration of a miR-495 antagomir. Moreover, there was an increased expression of AKT1. These findings indicate that miR-495 induces OA by targeting AKT1 and regulating the AKT/mTOR pathway. Therefore, miR-495 may be a prospective target for OA treatment.
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Identifiers
31105831PMC6511756W2982947628What 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.