IL‐1β‐induced miR‐34a up‐regulation inhibits Cyr61 to modulate osteoarthritis chondrocyte proliferation through ADAMTS‐4

Yang, Bo; Ni, Jiangdong; Long, Hui; Huang, Jun; Cheng, Yang; Huang, Xianzhe

doi:10.1002/jcb.26600

Cited by 20 publications

(15 citation statements)

References 50 publications

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“…Additionally, miR-34a expression was induced by IL-1β in OA [31]. Consistent with previous studies [35], we found that The mRNA a and protein b expression of SYVN1 was detected in OA cells (IL-1β) transfected with anti-NC, anti-miR-34a-5p, anti-miR-34a-5p + scramble and anti-miR-34a-5p + siSYVN1 by qRT-PCR and western blot. c Cell proliferation was measured in OA cells (IL-1β) transfected with anti-NC, anti-miR-34a-5p, anti-miR-34a-5p + scramble and anti-miR-34a-5p + siSYVN1 after transfection 24 h, 48 h, 72 h by MTT assay.…”

Section: Discussionsupporting

confidence: 91%

LncRNA SNHG7/miR-34a-5p/SYVN1 axis plays a vital role in proliferation, apoptosis and autophagy in osteoarthritis

et al. 2020

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Background: Osteoarthritis (OA) is one of the most common rheumatic diseases of which clinical symptoms includes swelling, synovitis and inflammatory pain, affect patients' daily life. It was reported that non-coding RNAs play vital roles in OA. However, the regulation mechanism of ncRNA in OA pathogenesis has not been fully elucidated. Methods: The expression of SNHG7, miR-34a-5p and SYVN1 was detected using qRT-PCR in tissues, serum and cells. The protein expression of SYVN1, PCNA, cleavage-caspase 3, beclin1 and LC3 were measured using western blot. The RNA immunoprecipitation (RIP), RNA pulldown, and luciferase reporter assays were used to verify the relationship between SNHG7, miR-34a-5p and SYVN1. The MTT and flow cytometry assay was performed to detected cell proliferation and cell apoptosis respectively. Results: In this study, SNHG7 and SYVN1 expression were down-regulated, but miR-34a-5p was up-regulated in OA tissues and IL-1β treated cells compared with normal tissues and chondrocyte. Functional investigation revealed that up-regulated SNHG7 or down-regulated miR-34a-5p could promote cell proliferation and inhibit cell apoptosis and autophagy in OA cells. More than that, RIP, pulldown and luciferase reporter assay was applied to determine that miR-34a-5p was a target miRNA of SNHG7 and SYVN1 was a target mRNA of miR-34-5p. Rescue experiments showed that overexpression of miR-34a reversed high expression of SNHG7-mediated suppression of apoptosis and autophagy as well as promotion of proliferation, while its knockdown inhibited cell apoptosis and autophagy and promoted cell proliferation which could be impaired by silencing SYVN1. In addition, SNHG7 regulated SYVN1 through sponging miR-34a-5p. Conclusion: SNHG7 sponged miR-34a-5p to affect cell proliferation, apoptosis and autophagy through targeting SYVN1 which provides a novel sight into the pathogenesis of OA.

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Section: Discussionsupporting

confidence: 91%

LncRNA SNHG7/miR-34a-5p/SYVN1 axis plays a vital role in proliferation, apoptosis and autophagy in osteoarthritis

et al. 2020

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“…Both miR-34a and miR-34b are upregulated in human knee OA AC compared to normal AC [ 147 , 181 ]. Also primary cell cultures of human knee OA AC show increased miR-34a expression compared to healthy controls [ 182 ].…”

Section: Mirna Regulation Of Fibroblast Growth Factor 2 Transformmentioning

confidence: 99%

“…Another target is cysteine-rich angiogenic inducer 61 ( CYR61 ), which inhibits ADAMTS-4. Indeed, upregulation of miR-34a by rIL-1β promotes ADAMTS-4 expression in human AC cells [ 181 ]. In human primary immortalized fibroblasts the MAPK activated transcription factor ELK1 is involved in miR-34a expression [ 183 ].…”

Section: Mirna Regulation Of Fibroblast Growth Factor 2 Transformmentioning

confidence: 99%

Onset and Progression of Human Osteoarthritis—Can Growth Factors, Inflammatory Cytokines, or Differential miRNA Expression Concomitantly Induce Proliferation, ECM Degradation, and Inflammation in Articular Cartilage?

Boehme,

Rolauffs

2018

IJMS

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Osteoarthritis (OA) is a degenerative whole joint disease, for which no preventative or therapeutic biological interventions are available. This is likely due to the fact that OA pathogenesis includes several signaling pathways, whose interactions remain unclear, especially at disease onset. Early OA is characterized by three key events: a rarely considered early phase of proliferation of cartilage-resident cells, in contrast to well-established increased synthesis, and degradation of extracellular matrix components and inflammation, associated with OA progression. We focused on the question, which of these key events are regulated by growth factors, inflammatory cytokines, and/or miRNA abundance. Collectively, we elucidated a specific sequence of the OA key events that are described best as a very early phase of proliferation of human articular cartilage (AC) cells and concomitant anabolic/catabolic effects that are accompanied by incipient pro-inflammatory effects. Many of the reviewed factors appeared able to induce one or two key events. Only one factor, fibroblast growth factor 2 (FGF2), is capable of concomitantly inducing all key events. Moreover, AC cell proliferation cannot be induced and, in fact, is suppressed by inflammatory signaling, suggesting that inflammatory signaling cannot be the sole inductor of all early OA key events, especially at disease onset.

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“…The prevalence of OA worldwide is staggeringly high with an estimated over 250 million people affected and with a lifetime risk for worsening to knee OA of approximately 40% [3]. Chondrocyte, a primary cell type of articular cartilage which occupies approximately 1% of total cartilage volume, is essential for retaining the dynamic equilibrium between catabolism and anabolism of the extracellular matrix in articular cartilage and has been deemed as one of the indispensable regulators of OA pathogenesis [4,5]. Declining cell number and cell viability of chondrocytes is implicated in the progression and advancement of OA [6].…”

Section: Introductionmentioning

confidence: 99%

Potential of miR-25-3p in protection of chondrocytes: emphasis on osteoarthritis

Deng

2021

Folia Histochem Cytobiol.

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Introduction. Osteoarthritis (OA) is the most prevailing musculoskeletal dysfunction triggered by lesions in synovial membranes and articular cartilage. MicroRNAs (miRNAs) have emerged as crucial regulators participated in many biological courses, such as osteoarthritis. This study was undertaken to address the role of miR-25-3p in the apoptosis of rat chondrocytes under an OA-like condition and its underlying mechanism. Material and methods. OA cellular model was established in rat chondrocytes by TNF-α induction. Then, qRT-PCR and Western blotting were utilized for evaluation of the expressions of miR-25-3p and insulin-like growth factor-binding protein 7 (IGFBP7), CCK-8 assay for inspection of chondrocyte viability, flow cytometry for assessment of cell apoptosis rate, Western blotting for the detection of cleaved caspase-3 level and dual-luciferase reporter gene assay for verification of the targeting relationship between miR-25-3p and IGFBP7. Results. The miR-25-3p expression was decreased and IGFBP7 was elevated in TNF-α-induced rat chondrocytes. The miR-25-3p inhibited chondrocyte apoptosis and IGFBP7 promoted apoptosis as evidenced by enhanced cell viability and suppressed cell apoptosis in OA chondrocytes after miR-25-3p overexpression or IGFBP7 knockdown. The miR-25-3p facilitated chondrocyte viability and repressed cell apoptosis in OA by negatively regulating IGFBP7. Conclusions. MiR-25-3p negatively regulates IGFBP7 to promote chondrocyte proliferation and restrain chondrocyte apoptosis. Our findings suggest that the regulation of IGFBP7 by miR-25-3p may emerge as a novel therapeutic regimen for OA.

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IL‐1β‐induced miR‐34a up‐regulation inhibits Cyr61 to modulate osteoarthritis chondrocyte proliferation through ADAMTS‐4

Cited by 20 publications

References 50 publications

LncRNA SNHG7/miR-34a-5p/SYVN1 axis plays a vital role in proliferation, apoptosis and autophagy in osteoarthritis

LncRNA SNHG7/miR-34a-5p/SYVN1 axis plays a vital role in proliferation, apoptosis and autophagy in osteoarthritis

Onset and Progression of Human Osteoarthritis—Can Growth Factors, Inflammatory Cytokines, or Differential miRNA Expression Concomitantly Induce Proliferation, ECM Degradation, and Inflammation in Articular Cartilage?

Potential of miR-25-3p in protection of chondrocytes: emphasis on osteoarthritis

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