TRIM59 attenuates IL-1β-driven cartilage matrix degradation in osteoarthritis via direct suppression of NF-κB and JAK2/STAT3 signaling pathway

Teng, Yue; Ni, Gang; Zhang, Wen; Hua, Jiong; Sun, Lin; Zheng, Min; Dong, Qirong; Huang, Weijie

doi:10.1016/j.bbrc.2020.05.130

Cited by 14 publications

(11 citation statements)

References 30 publications

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“…The present study verified that JAK2 is a target gene of miR-369-3p, and overexpression of miR-369-3p restrained JAK2 expression in OA chondrocytes. In addition, previous studies have confirmed that the JAK2/STAT3 signaling pathway participates in OA development [ 30 , 43 ]. The results of the present study demonstrated that addition of miR-369-3p suppressed JAK2 protein expression, thus inhibiting the activation of JAK2/STAT3 signaling.…”

Section: Discussionmentioning

confidence: 81%

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Long non-coding RNA musculin antisense RNA 1 promotes proliferation and suppresses apoptosis in osteoarthritic chondrocytes via the microRNA-369-3p/Janus kinase-2/ signal transducers and activators of transcription 3 axis

2022

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Increasing evidence indicates that long non-coding RNAs (lncRNAs) play critical roles in osteoarthritis (OA). The present study aimed to investigate the underlying molecular mechanism of lncRNA musculin antisense RNA 1 (MSC-AS1) in OA. RT-qPCR was used to detect MSC-AS1 levels in cartilage tissues from patients with OA. The effects of MSC-AS1 knockdown on the viability and apoptosis in OA were evaluated via CCK-8 and TUNEL assays. The StarBase database was used to predict the binding sites between microRNA (miR)-369-3p and MSC-AS1 or JAK2, which were confirmed via the dual-luciferase reporter assay. The results demonstrated that MSC-AS1 expression was downregulated in OA. Functional analysis indicated that the addition of MSC-AS1 promoted viability and inhibited inflammation and the apoptosis of chondrocytes. In addition, MSC-AS1 regulated the survival of OA chondrocytes by sponging miR-369-3p. JAK2 was confirmed as a direct target of miR-369-3p, and MSC-AS1 regulated JAK2/STAT3 signaling via miR-369-3p in OA chondrocytes. Taken together, our results suggest that MSC-AS1 may regulate the miR-369-3p/JAK2/STAT3 signaling pathway to accelerate the viability, and inhibit inflammation and cell apoptosis in OA chondrocytes.

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Section: Discussionmentioning

confidence: 81%

“…Previous studies have reported that JAK2/STAT3 signaling plays a crucial role in OA [ 29 , 30 ]. The regulatory role of the MSC-AS1/miR-369-3p/JAK2/STAT3 signaling pathway in OA was further investigated.…”

Section: Msc-as1 Sponges Mir-369-3p To Modulate the Jak2/stat3 Signaling Pathway In Oa Chondrocytesmentioning

confidence: 99%

Long non-coding RNA musculin antisense RNA 1 promotes proliferation and suppresses apoptosis in osteoarthritic chondrocytes via the microRNA-369-3p/Janus kinase-2/ signal transducers and activators of transcription 3 axis

2022

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“…Reports have indicated that the JAK/STAT pathway can be regulated by some TRIMs ( Rajsbaum et al, 2014b ; Teng et al, 2020 ; van Tol et al, 2020 ). TRIM6 was found to modulate IFNα/β-induced JAK/STAT signaling for antiviral response via cooperation with E2-ubiquitin conjugase UbE2K and promotion of the synthesis of unanchored K48-linked polyubiquitin chains, which activated IKKε for subsequent STAT1 phosphorylation ( Rajsbaum et al, 2014b ).…”

Section: Trim Regulation Of Innate Immune Responsementioning

confidence: 99%

“…Its expression and function are dependent on TRIM6 activity ( van Tol et al, 2020 ). TRIM59 interacts with STAT1 by recruiting much more PIAS1 to suppress the activation of STAT1, and it also suppresses IL-1β-induced activation of the JAK2/STAT3 pathway ( Su et al, 2020 ; Teng et al, 2020 ). TRIM8 enhances IL-6-dependent activation of STAT3 by degradation of PIAS3, which is the protein inhibitor of activated STAT3 ( Okumura et al, 2010 ).…”

Section: Trim Regulation Of Innate Immune Responsementioning

confidence: 99%

Regulation of Tripartite Motif-Containing Proteins on Immune Response and Viral Evasion

Zhang

Wang

2021

Front. Microbiol.

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Tripartite motif-containing proteins (TRIMs), exhibiting ubiquitin E3 ligase activity, are involved in regulation of not only autophagy and apoptosis but also pyrotosis and antiviral immune responses of host cells. TRIMs play important roles in modulating signaling pathways of antiviral immune responses via type I interferon, NF-κB, Janus kinase/signal transducer and activator of transcription (JAK/STAT), and Nrf2. However, viruses are able to antagonize TRIM activity or evenly utilize TRIMs for viral replication. This communication presents the current understanding of TRIMs exploited by viruses to evade host immune response.

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“…Of note, miR-15a-5p has been demonstrated to show downregulated expression patterns in endometriotic tissues and Ect-ESCs-derived extracellular vesicles [18,19], and inhibition of miR-15a-5p promotes ESC migration and invasion [20]. Moreover, TRIM59, a member of the TRIM protein family that is associated with autophagy, immunity, anti-virus, and carcinogenesis and plays roles in the pathogenesis of osteoarthritis, sepsis, and myocardial ischemia-reperfusion injury [21][22][23][24][25], and TRIM59 overexpression can facilitate the invasion of ectopic ESCs (Ect-ESCs) [26]. Nevertheless, the ceRNA network of lncRNA BANCR/miR-590-5p/TRIM59 in EM has not been studied before and warrants further investigation.…”

Section: Introductionmentioning

confidence: 99%

LncRNA BANCR Promotes Endometrial Stromal Cell Proliferation and Invasion in Endometriosis via the miR-15a-5p/TRIM59 Axis

Liu

Bai

et al. 2022

International Journal of Genomics

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Long non-coding RNA (LncRNA) emerges as a regulator in various diseases, including endometriosis (EM). This study aims to uncover the role of long non-coding RNA BRAF-activated non-protein coding RNA (lncRNA BANCR)-mediated competing endogenous RNA mechanism in endometrial stromal cell (ESC) proliferation and invasion in EM by regulating miR-15a-5p/TRIM59. ESCs were isolated from eutopic and ectopic endometrial tissues, followed by the determination of Cytokeratin 19 and Vimentin expressions in cells. Then, expressions of lncRNA BANCR, microRNA (miR)-15a-5p, and tripartite motif-containing 59 (TRIM59) in tissues and cells were determined by real-time quantitative polymerase chain reaction or Western blot assay, and cell proliferation and invasion were evaluated by cell counting kit-8 and transwell assays. After that, the subcellular localization of lncRNA BANCR and binding of miR-15a-5p to lncRNA BANCR or TRIM59 were analyzed. LncRNA BANCR was upregulated in ectopic endometrial tissues and ectopic ESCs (Ect-ESCs). Silencing lncRNA BANCR suppressed Ect-ESC proliferation and invasion. LncRNA BANCR inhibited miR-15a-5p to promote TRIM59 expression. miR-15a-5p downregulation or TRIM59 overexpression both reversed the effects of silencing lncRNA BANCR on Ect-ESC proliferation and invasion. In summary, our findings suggested that lncRNA BANCR facilitated Ect-ESC proliferation and invasion by inhibiting miR-15a-5p and promoting TRIM59.

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TRIM59 attenuates IL-1β-driven cartilage matrix degradation in osteoarthritis via direct suppression of NF-κB and JAK2/STAT3 signaling pathway

Cited by 14 publications

References 30 publications

Long non-coding RNA musculin antisense RNA 1 promotes proliferation and suppresses apoptosis in osteoarthritic chondrocytes via the microRNA-369-3p/Janus kinase-2/ signal transducers and activators of transcription 3 axis

Long non-coding RNA musculin antisense RNA 1 promotes proliferation and suppresses apoptosis in osteoarthritic chondrocytes via the microRNA-369-3p/Janus kinase-2/ signal transducers and activators of transcription 3 axis

Regulation of Tripartite Motif-Containing Proteins on Immune Response and Viral Evasion

LncRNA BANCR Promotes Endometrial Stromal Cell Proliferation and Invasion in Endometriosis via the miR-15a-5p/TRIM59 Axis

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