Epigenetics in osteoarthritis: Novel spotlight

Fathollahi, Anwar; Aslani, Saeed; Jamshidi, Ahmadreza; Mahmoudi, Mahdi

doi:10.1002/jcp.28020

Cited by 49 publications

(32 citation statements)

References 150 publications

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“…MiRNA has been widely investigated for their role in gene regulation; by binding to mRNA 3′-UTRs, miRNA can affect many protein-encoding genes at the post-transcriptional levels [22,24,57]. It is proved that some miRNA are differentially expressed in OA cartilage samples with respect to normal ones, demonstrating their role in the development and progression of OA [23,24,26].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA Mediate Visfatin and Resistin Induction of Oxidative Stress in Human Osteoarthritic Synovial Fibroblasts Via NF-κB Pathway

Cheleschi

Gallo

Barbarino

et al. 2019

IJMS

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Synovial membrane inflammation actively participate to structural damage during osteoarthritis (OA). Adipokines, miRNA, and oxidative stress contribute to synovitis and cartilage destruction in OA. We investigated the relationship between visfatin, resistin and miRNA in oxidative stress regulation, in human OA synovial fibroblasts. Cultured cells were treated with visfatin and resistin. After 24 h, we evaluated various pro-inflammatory cytokines, metalloproteinases (MMPs), type II collagen (Col2a1), miR-34a, miR-146a, miR-181a, antioxidant enzymes, and B-cell lymphoma (BCL)2 by qRT-PCR, apoptosis and mitochondrial superoxide production by cytometry, p50 nuclear factor (NF)-κB by immunofluorescence. Synoviocytes were transfected with miRNA inhibitors and oxidative stress evaluation after adipokines stimulus was performed. The implication of NF-κB pathway was assessed by the use of a NF-κB inhibitor (BAY-11-7082). Visfatin and resistin significantly up-regulated gene expression of interleukin (IL)-1β, IL-6, IL-17, tumor necrosis factor (TNF)-α, MMP-1, MMP-13 and reduced Col2a1. Furthermore, adipokines induced apoptosis and superoxide production, the transcriptional levels of BCL2, superoxide dismutase (SOD)-2, catalase (CAT), nuclear factor erythroid 2 like 2 (NRF2), miR-34a, miR-146a, and miR-181a. MiRNA inhibitors counteracted adipokines modulation of oxidative stress. Visfatin and resistin effects were suppressed by BAY-11-7082. Our data suggest that miRNA may represent possible mediators of oxidative stress induced by visfatin and resistin via NF-κB pathway in human OA synoviocytes.

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Section: Discussionmentioning

confidence: 99%

MicroRNA Mediate Visfatin and Resistin Induction of Oxidative Stress in Human Osteoarthritic Synovial Fibroblasts Via NF-κB Pathway

Cheleschi

Gallo

Barbarino

et al. 2019

IJMS

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“…(b) development and remodeling that entail orderly transitions from stem cell proliferation to differentiation; (c) phenotypic variation that results from changes in the timing of developmental transitions, or heterochrony; (d) adaptation that can arise quite rapidly; and (e) an "environmental sensitivity" and adaptability of this complex system that is mediated by epigenetic modification of gene networks, rather than by gene mutations or constant evolution of entirely new signaling pathways over geological time. This last point has been illustrated by various studies (Fathollahi, Aslani, Jamshidi, & Mahmoudi, 2019;Reppe, Datta, & Gautvik, 2017;Van Meurs, Boer, Lopez-Delgado, & Riancho, 2019;Vrtacnik, Mare, & Ostanek, 2014).…”

mentioning

confidence: 80%

Osteoarthritis from evolutionary and mechanistic perspectives

Tangredi

Lawler

2019

The Anatomical Record

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Developmental osteogenesis and the pathologies associated with tissues that normally are mineralized are active areas of research. All of the basic cell types of skeletal tissue evolved in early aquatic vertebrates. Their characteristics, transcription factors, and signaling pathways have been conserved, even as they adapted to the challenge imposed by gravity in the transition to terrestrial existence. The response to excess mechanical stress (among other factors) can be expressed in the pathologic phenotype described as osteoarthritis (OA). OA is mediated by epigenetic modification of the same conserved developmental gene networks, rather than by gene mutations or new chemical signaling pathways. Thus, these responses have their evolutionary roots in morphogenesis. Epigenetic channeling and heterochrony, orchestrated primarily by micro-RNAs, maintain the sequence of these responses, while allowing variation in their timing that depends at least partly on the life history of the individual.

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“…Recently, it has been reported that OA is not the absolute consequence of joint mechanical use. The implication of inflammatory cytokines contributes to the development and progression of OA 10. Cartilage, subchondral bone, and synovium probably have critical roles in OA pathogenesis.…”

Section: Introductionmentioning

confidence: 99%

“…Epigenetic modification has been involved in OA pathogenesis at all of its levels, including DNA methylation, histone modification, miRNAs, and long non-coding RNA 10. Accumulating evidence has demonstrated that miRNAs play a crucial role as regulators of cartilage biology and in OA pathogenesis 14.…”

Section: Introductionmentioning

confidence: 99%

<p>TMF inhibits miR-29a/Wnt/β-catenin signaling through upregulating Foxo3a activity in osteoarthritis chondrocytes</p>

Huang¹,

Chen²,

Shi³

et al. 2019

DDDT

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Background: miR-29a, a downstream factor of Wnt/β-catenin signaling, promotes the activity of the Wnt/β-catenin signaling in a positive feedback loop. Our previous work showed that 5,7,3ʹ,4ʹ-tetramethoxyflavone (TMF), a major constituent from Murraya exotica L., exhibited chondroprotective activity by inhibiting the activity of Wnt/β-catenin signaling. Purpose: To investigate whether TMF showed the inhibitory effects on miR-29a/β-catenin signaling by up regulation of Foxo3a expression. Methods: Rat knee OA models were duplicated by using Hulth’s method. TMF (5 μg/mL and 20 μg/mL) was used for administration to cultured cells, which were isolated from the rat cartilages. Analysis of chondrocytes apoptosis, gene expression, and protein expression were conducted. In addition, miR-29a mimics and pcDNA3.1(+)-Foxo3a vector were used for transfection, luciferase reporter assay for detecting the activity of Wnt/β-catenin signaling, and co-immunoprecipitation for determining proteins interaction. Results: TMF down regulated miR-29a/β-catenin signaling activity and cleaved caspase-3 expression and up regulated Foxo3a expression in OA rat cartilages. In vitro, miR-29a mimics down regulated the expression of Foxo3a and up regulated the activity of Wnt/β-catenin signaling and cleaved caspase-3 expression. TMF ameliorated miR-29a/β-catenin-induced chondrocytes apoptosis by up regulation of Foxo3a expression. Conclusion: TMF exhibited chondroprotective activity by up regulating Foxo3a expression and subsequently inhibiting miR-29a/Wnt/β-catenin signaling activity.

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Epigenetics in osteoarthritis: Novel spotlight

Cited by 49 publications

References 150 publications

MicroRNA Mediate Visfatin and Resistin Induction of Oxidative Stress in Human Osteoarthritic Synovial Fibroblasts Via NF-κB Pathway

MicroRNA Mediate Visfatin and Resistin Induction of Oxidative Stress in Human Osteoarthritic Synovial Fibroblasts Via NF-κB Pathway

Osteoarthritis from evolutionary and mechanistic perspectives

<p>TMF inhibits miR-29a/Wnt/β-catenin signaling through upregulating Foxo3a activity in osteoarthritis chondrocytes</p>

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