<i>Retracted</i>: microRNA‐590‐5p targets transforming growth factor β1 to promote chondrocyte apoptosis and autophagy in response to mechanical pressure injury

Wang, Jun; Song, Wei; Ma, Tao; Wang, Kunzheng

doi:10.1002/jcb.27315

Cited by 9 publications

(9 citation statements)

References 26 publications

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“…For example, Lian et al [ 27 ] showed that miR-128a represses chondrocyte autophagy and exacerbates knee OA by disrupting autophagy related 12 gene. Wang et al [ 28 ] indicated that mR-590-5p targets transforming growth factor β1 to promote chondrocytes apoptosis and autophagy in response to mechanical pressure injury. Yu et al [ 29 ] demonstrated that inhibition of miR-126 protects chondrocytes from IL-1β induced inflammation via up-regulation of Bcl-2.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-197 regulates chondrocyte proliferation, migration, and inflammation in pathogenesis of osteoarthritis by targeting EIF4G2

et al. 2020

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Recent studies have demonstrated that microRNAs (miRNAs) are involved in many pathological conditions including osteoarthritis (OA). In this study, we aimed to investigate the role of miR-197 in OA and the potential molecular mechanism. The expression levels of miR-197 was detected by quantitative real-time PCR analysis. Cell proliferation and migration abilities were performed by MTT and transwell assays. The concentrations of inflammatory cytokines, including IL-1β, IL-6, and TNF-α, were detect using ELISA assay. Furthermore, luciferase reporter and rescue assays were applied to identify the functional target gene of miR-197 in OA. The results showed that miR-197 expression was significantly downregulated in the OA cartilage tissues compared with normal cartilage tissues, accompanied by upregulation of EIF4G2 expression. An inverse correlation was found between EIF4G2 and miR-197 expressions in OA cartilage tissues. Treatment with miR-197 mimics promoted the growth and migration abilities of chondrocytes, while miR-197 inhibitors induced the opposite effects. Furthermore, restoration of miR-197 significantly decreased IL-1β, IL-6, and TNF-α expression, whereas knockdown of miR-197 led to a induction in these inflammatory mediators. Moreover, EIF4G2 was predicted and confirmed as a directly target of miR-197. Overexpressed miR-197 could downregulate EIF4G2 expression in chondrocytes, while miR-197 knockdown could elevate EIF4G2 expression. Additionally, EIF4G2 overexpression reversed the effects of miR-197 mimics on chondrocytes proliferation, migration and inflammation. Taken together, our study demonstrated that miR-197 promotes chondrocyte proliferation, increases migration, and inhibits inflammation in the pathogenesis of OA by targeting EIF4G2, indicating the potential therapeutic targets of the miR-197/EIF4G2 axis for OA treatment.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-197 regulates chondrocyte proliferation, migration, and inflammation in pathogenesis of osteoarthritis by targeting EIF4G2

et al. 2020

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“…Numerous studies have shown that there may be a common regulatory factor between autophagy and apoptosis. In the model of focal cerebral ischemia and ischemic injury, Beclin 1 may be involved in the activation of caspase-3, and the anti-apoptotic protein Bcl-2 binds to Beclin 1 to block autophagy (Ciechomska et al, 2009; Yang et al, 2017; Ding et al, 2018; Wang J. et al, 2018). In the present study, we established a rat model of CCH and took samples at different timepoints of resveratrol treatment.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol Activates Autophagy via the AKT/mTOR Signaling Pathway to Improve Cognitive Dysfunction in Rats With Chronic Cerebral Hypoperfusion

Wang¹,

He²,

Pan³

et al. 2019

Front. Neurosci.

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Chronic cerebral hypoperfusion (CCH) is a main cause of vascular dementia and is also an etiological factor of neurological diseases and mental disorders. However, few treatments are available for CCH, and new medications are needed. In the present study, we employed a rat model of CCH that was based on bilateral common carotid artery occlusion and investigated the therapeutic effects of resveratrol and its detailed mechanism of action. We evaluated neurological deficit scores and performed the Morris water maze test, hematoxylin and eosin staining, TUNEL staining, enzyme-linked immunosorbent assays, and Western blot. Resveratrol reduced neurological deficit scores in CCH rats and reduced pathological damage in the frontal cortex and hippocampus. Resveratrol activated autophagy and inhibited the expression of AKT/mechanistic target of rapamycin (mTOR) signaling pathway-related proteins. Treatment with a phosphoinositide-3 kinase inhibitor reversed the protective effect of resveratrol. These findings suggest that resveratrol improves cognitive function in a rat model of CCH and reduces oxidative stress-induced neuronal damage in the frontal cortex and hippocampus by activating autophagy and inhibiting neuronal apoptosis. These effects may be regulated by the AKT/mTOR signaling pathway.

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“…A study by De Palma et al [56] reported that mechanical loading downregulated MIR-155 and MIR-181a in OA cartilage and activated the NF-κB pathway. Mechanical loading increased MIR-590-5p expression and activated TGF-β thereby enhancing chondrocyte apoptosis and autophagy [57]. Overloading activates the IL-1 β pathway and ADAMT5 and upregulates MIR-145 to promote ECM degradation [16].…”

Section: Microrna and Osteoarthritismentioning

confidence: 99%

Molecular mechanisms of mechanical load-induced osteoarthritis

Fang

Zhou

Jin

et al. 2021

International Orthopaedics (SICOT)

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Introduction Mechanical loading enhances the progression of osteoarthritis. However, its molecular mechanisms have not been established. Objective The aim of this review was to summarize the probable mechanisms of mechanical load-induced osteoarthritis. Methods A comprehensive search strategy was used to search PubMed and EMBASE databases (from the 15th of January 2015 to the 20th of October 2020). Search terms included “osteoarthritis”, “mechanical load”, and “mechanism”. Results Abnormal mechanical loading activates the interleukin-1β, tumour necrosis factor-α, nuclear factor kappa-B, Wnt, transforming growth factor-β, microRNAs pathways, and the oxidative stress pathway. These pathways induce the pathological progression of osteoarthritis. Mechanical stress signal receptors such as integrin, ion channel receptors, hydrogen peroxide-inducible clone-5, Gremlin-1, and transient receptor potential channel 4 are present in the articular cartilages. Conclusion This review highlights the molecular mechanisms of mechanical loading in inducing chondrocyte apoptosis and extracellular matrix degradation. These mechanisms provide potential targets for osteoarthritis prevention and treatment.

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Retracted: microRNA‐590‐5p targets transforming growth factor β1 to promote chondrocyte apoptosis and autophagy in response to mechanical pressure injury

Cited by 9 publications

References 26 publications

MicroRNA-197 regulates chondrocyte proliferation, migration, and inflammation in pathogenesis of osteoarthritis by targeting EIF4G2

MicroRNA-197 regulates chondrocyte proliferation, migration, and inflammation in pathogenesis of osteoarthritis by targeting EIF4G2

Resveratrol Activates Autophagy via the AKT/mTOR Signaling Pathway to Improve Cognitive Dysfunction in Rats With Chronic Cerebral Hypoperfusion

Molecular mechanisms of mechanical load-induced osteoarthritis

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