ArticleExperimental and therapeutic medicine2018
miR-4262 regulates chondrocyte viability, apoptosis, autophagy by targeting SIRT1 and activating PI3K/AKT/mTOR signaling pathway in rats with osteoarthritis.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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28 citing papers in PubMed, 56 citations in OpenAlex.
- Single-cell RNA sequencing identifies the expression of hemoglobin in chondrocyte cell subpopulations in osteoarthritis.BMC molecular and cell biology · 2024Article
- A new perspective on the autophagic and non-autophagic functions of the GABARAP protein family: a potential therapeutic target for human diseases.Molecular and cellular biochemistry · 2024Review
- Chondrocyte autophagy mechanism and therapeutic prospects in osteoarthritis.Frontiers in cell and developmental biology · 2024Review
- Advances in understanding effects of miRNAs on apoptosis, autophagy, and pyroptosis in knee osteoarthritis.Molecular genetics and genomics : MGG · 2023Review
- Autophagy in the pathogenesis and therapeutic potential of post-traumatic osteoarthritis.Burns & trauma · 2023Review
- Circ-NCX1 inhibits LPS-induced chondrocyte apoptosis by regulating the miR-133a/SIRT1 axis.The Kaohsiung journal of medical sciences · 2022Article
- High TRB3 expression induces chondrocyte autophagy and senescence in osteoarthritis cartilage.Aging · 2022Article
- Exploring the role of non-coding RNAs in autophagy.Autophagy · 2022Review
- Corosolic Acid Protects Rat Chondrocytes Against IL-1β-Induced ECM Degradation by Activating Autophagy via PI3K/AKT/mTOR Pathway and Ameliorates Rat Osteoarthritis.Drug design, development and therapy · 2022Article
- Moderate-intensity treadmill running relieves motion-induced post-traumatic osteoarthritis mice by up-regulating the expression of lncRNA H19.Biomedical engineering online · 2021Article
- Polysaccharide from Angelica sinensis attenuates SNP-induced apoptosis in osteoarthritis chondrocytes by inducing autophagy via the ERK1/2 pathway.Arthritis research & therapy · 2021Article
- Regulation of autophagy by miRNAs in human diseases.The Nucleus : an international journal of cytology and allied topics · 2021Review
- CRNDE Contributes Cervical Cancer Progression by Regulating miR-4262/ZEB1 Axis.OncoTargets and therapy · 2021Article
- AMPK Signaling in Energy Control, Cartilage Biology, and Osteoarthritis.Frontiers in cell and developmental biology · 2021Review
- UVA influenced the SIRT1-miR-27a-5p-SMAD2-MMP1/COL1/BCL2 axis in human skin primary fibroblasts.Journal of cellular and molecular medicine · 2020Article
- Mechanism underlying the significant role of the miR-4262/SIRT1 axis in children with inflammatory bowel disease.Experimental and therapeutic medicine · 2020Article
- miR-122/SIRT1 axis regulates chondrocyte extracellular matrix degradation in osteoarthritis.Bioscience reports · 2020Article
- SIRT1 directly activates autophagy in human chondrocytes.Cell death discovery · 2020Article
- Identification of the lncRNA-miRNA-mRNA network associated with gastric cancer via integrated bioinformatics analysis.Oncology letters · 2019Article
- Chondro-protective effects of polydatin in osteoarthritis through its effect on restoring dysregulated autophagy via modulating MAPK, and PI3K/Akt signaling pathways.Scientific reports · 2019Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to investigate the effect and underlying mechanism of microRNA (miR)-4262 in the development of osteoarthritis (OA) in rats. Primary chondrocytes were separated from Sprague-Dawley rats and then treated with tumor necrosis factor-α (TNF-α). The level of miR-4262 was detected in TNF-α-treated chondrocytes, and then the miR-4262 or its target gene sirtuin type 1 (SIRT1) level was overexpressed, or knocked down. Furthermore, cell viability, cell apoptosis, cell autophagy and matrix synthesis, as well as the expressions of proteins associated with the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway were detected. miR-4262 was significantly overexpressed in TNF-α-treated chondrocytes compared with untreated cells (P<0.05). TNF-α treatment or miR-4262 overexpression significantly decreased cell viability, autophagy-related proteins levels and matrix synthesis-related proteins levels, as well as increased the apoptotic rate in chondrocytes (P<0.05). Overexpression of SIRT1 significantly increased cell viability, autophagy-related proteins levels and matrix synthesis-related proteins levels, as well as decreased the apoptotic rate in TNF-α-treated chondrocytes (P<0.05). In addition, the effects of miR-4262 on cell viability, cell apoptosis, cell autophagy and matrix synthesis were inhibited by SIRT1 (P<0.05). Furthermore, upregulated miR-4262 remarkably increased the expressions of phosphorylated (p)-PI3K, p-AKT and p-mTOR (P<0.05) in TNF-α treated chondrocytes. The present study revealed that the upregulation of miR-4262 may promote the occurrence and development of OA in rats by regulating cell viability, cell apoptosis, cell autophagy, and matrix synthesis. Furthermore, these roles of miR-4262 may be associated with PI3K/AKT/mTOR signaling pathway.
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