2019
DOI: 10.3390/cells8080874
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MicroRNA-34a and MicroRNA-181a Mediate Visfatin-Induced Apoptosis and Oxidative Stress via NF-κB Pathway in Human Osteoarthritic Chondrocytes

Abstract: Current evidence suggests a complex interaction between adipokines and microRNA (miRNA) in osteoarthritis (OA) pathogenesis. The present study explored the role of miR-34a and miR-181a in regulating apoptosis and oxidative stress induced by visfatin in human OA chondrocytes. Chondrocytes were transfected with miR-34a and miR-181a inhibitors and stimulated with visfatin for 24 h, in the presence of nuclear factor (NF)-κB inhibitor (BAY-11-7082, 2 h pre-incubation). Apoptosis and reactive oxygen species (ROS) pr… Show more

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Cited by 62 publications
(57 citation statements)
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“…We demonstrated an excessive mitochondrial ROS production following the exposure of OA chondrocytes to continuous HP of 10 MPa, while a positive reduction in cells subjected to cyclic low HP of 5 MPa was observed. However, our results revealed that the overproduction of ROS was associated to the increased expression levels of antioxidant factors, SOD-2 and NRF2, maybe as a radical scavenging mechanism activated by the cells against the excessive amount of ROS [29,30,49]. Indeed, since the deleterious effects of abundant ROS sources, the antioxidant system, driven by NRF2 transcription factor, react to deactivate ROS and protect the cells from oxidative damage.…”
Section: Discussionmentioning
confidence: 70%
See 2 more Smart Citations
“…We demonstrated an excessive mitochondrial ROS production following the exposure of OA chondrocytes to continuous HP of 10 MPa, while a positive reduction in cells subjected to cyclic low HP of 5 MPa was observed. However, our results revealed that the overproduction of ROS was associated to the increased expression levels of antioxidant factors, SOD-2 and NRF2, maybe as a radical scavenging mechanism activated by the cells against the excessive amount of ROS [29,30,49]. Indeed, since the deleterious effects of abundant ROS sources, the antioxidant system, driven by NRF2 transcription factor, react to deactivate ROS and protect the cells from oxidative damage.…”
Section: Discussionmentioning
confidence: 70%
“…Indeed, since the deleterious effects of abundant ROS sources, the antioxidant system, driven by NRF2 transcription factor, react to deactivate ROS and protect the cells from oxidative damage. When activated, NRF2 is released from its repressive cytosolic protein Kelch-like ECH associated protein1 (KEAP1), translocates into the nucleus, and stimulates the expression of cytoprotective genes encoding antioxidant enzymes, such as SOD-2 and catalase, for neutralizing ROS species [21,29,30,49,50].…”
Section: Discussionmentioning
confidence: 99%
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“…Furthermore, Cheleschi et al indicated that visfatin significantly increased the expression levels of miR-34a and miR-181a via NF-κB pathway in human osteoarthritic chondrocytes. Moreover, visfatin led to the enhancement of expression levels of SOD2, CAT, Nrf2 and the production of O2 −• [177]. HOX transcript antisense RNA (HOTAIR), which is implicated in many diseases, was decreased in response to HG in cardiomyocytes and in the hearts of streptozotocin (STZ)-treated mice.…”
Section: Mirnas In Mets-a Link With Obesity and Insulin Resistance/hymentioning
confidence: 99%
“…In vitro studies were normally used to evaluate the effects and/or the mechanism of action of mechanical (such as hydrostatic pressure, mechanical compression, ultrasound, magnetic or electromagnetic fields) or chemical factors (cytokine, growth factors, adipokines, drugs, mineral elements, etc.) on cell or tissue morphology and metabolism (Cheleschi et al 2015;Cheleschi et al 2018;Cheleschi et al 2019a;Cheleschi et al 2019b;Collodel et al 2013;Fioravanti et al 2010;Kloesch et al 2011;Marrazzo et al 2019;Shams et al 2018).…”
Section: Whymentioning
confidence: 99%