The Role of Chondrocyte Hypertrophy and Senescence in Osteoarthritis Initiation and Progression

Rim, Yeri Alice; Nam, Yoonho; Ju, Ji Hyeon

doi:10.3390/ijms21072358

Cited by 210 publications

(173 citation statements)

References 105 publications

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“…The matrix that encapsulates chondrocytes plays a role of lubrication and mechanical support for cartilage joint. Although chondrocytes account for only 1% of the total cartilage volume, it plays an indelible role in maintaining the integrity of the matrix (Charlier et al, 2019;Rim et al, 2020). In fact, when certain factors act on the cartilage matrix and change its structure, chondrocytes can respond accordingly.…”

Section: Introductionmentioning

confidence: 99%

The Role of Autophagy in Osteoarthritis

Duan

Xie

Liu

2020

Front. Cell Dev. Biol.

112

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Chondrocytes are the only cell type in normal cartilage. The pathological changes of osteoarthritis (OA) mostly revolve around the apoptosis and dysfunction of chondrocytes. Autophagy, as an intracellular degradation system that maintains the steady state of energy metabolism in cells, has been shown to restore the function of damaged chondrocytes, alleviating the occurrence and progression of OA. In this review, we explored the relationship between autophagy and OA and the key molecules of autophagy pathway that regulate the progression of OA, providing new ideas for OA treatment by targeting autophagy.

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Section: Introductionmentioning

confidence: 99%

The Role of Autophagy in Osteoarthritis

Duan

Xie

Liu

2020

Front. Cell Dev. Biol.

112

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“…The molecular mechanism of OA is still indeterminate. Chondrocyte hypertrophy, senescence, and apoptosis are regarded as crucial biological events during the initiation and development of OA ( Charlier et al, 2016 ; Rim et al, 2020 ). In the present work, it was demonstrated that the MEG3/miR-9-5p/KLF4 axis was involved in regulating the viability, migration, apoptosis, and inflammatory response of chondrocytes.…”

Section: Discussionmentioning

confidence: 99%

LncRNA MEG3 Protects Chondrocytes From IL-1β-Induced Inflammation via Regulating miR-9-5p/KLF4 Axis

et al. 2021

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BackgroundOsteoarthritis (OA) is a chronic degenerative disease of the joints characterized by articular cartilage damage, subchondral bone remodeling, osteophyte formation, and inflammatory changes. This work aims to investigate the protective role of long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) against the apoptosis of chondrocytes.MethodsChondrocyte cell lines, CHON-001, and ATDC5 were treated with different doses of interleukin-1β (IL-1β) to mimic the inflammatory response during OA pathogenesis. Quantitative real-time polymerase chain reaction was performed to measure MEG3, miR-9-5p, and Krüppel-like factor 4 (KLF4) mRNA expression levels. MEG3 and KLF4 overexpression plasmids, MEG3 shRNA, miR-9-5p mimics, and miR-9-5p inhibitors were transfected into the cells. Cell counting kit-8, wound healing assay, and flow cytometry were conducted to determine cell viability, migration, and apoptotic rate. Dual-luciferase reporter assay was adopted to verify the targeting relationships among MEG3, miR-9-5p, and KLF4. Western blot was used to detect KLF4 protein expression. Enzyme-linked immunosorbent assay was employed to measure the levels of inflammatory factors.ResultsMEG3 expression in chondrocytes was down-regulated by the stimulation of IL-1β, and MEG3 negatively regulated miR-9-5p expression but positively regulated KLF4 expression. MEG3 overexpression strengthened the viability and migration of CHON-001 and ATDC5 cells but restrained the apoptosis and inflammatory response, while MEG3 knockdown had opposite effects. miR-9-5p inhibition or KLF4 overexpression could counteract the effects of MEG3 knockdown on chondrocytes. Besides that, MEG3 was proved to be a molecular sponge for miR-9-5p, and KLF4 was verified as the target of miR-9-5p.ConclusionMEG3 can promote chondrocyte proliferation and migration and inhibit apoptosis and inflammation by sponging miR-9-5p to induce KLF4 expression, which provides a promising therapy target for OA treatment.

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“…These changes in the cartilage environment ultimately reset the chondrocyte cell cycle and lead to abnormal chondrocyte proliferation and hypertrophic differentiation, which eventually results in chondrocyte apoptosis [ 50 , 51 ]. While the hypertrophic differentiation of chondrocytes is a normal pathway in developmental events, abnormal hypertrophic differentiation in adult cartilage is one of the causes of OA [ 54 ].…”

Section: Fibrosis and Oamentioning

confidence: 99%

The Role of Fibrosis in Osteoarthritis Progression

Rim

2020

Life

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Osteoarthritis (OA) is a chronic degenerative joint disease where the main characteristics include cartilage degeneration and synovial membrane inflammation. These changes in the knee joint eventually dampen the function of the joint and restrict joint movement, which eventually leads to a stage where total joint replacement is the only treatment option. While much is still unknown about the pathogenesis and progression mechanism of OA, joint fibrosis can be a critical issue for better understanding this disease. Synovial fibrosis and the generation of fibrocartilage are the two main fibrosis-related characteristics that can be found in OA. However, these two processes remain mostly misunderstood. In this review, we focus on the fibrosis process in OA, especially in the cartilage and the synovium tissue, which are the main tissues involved in OA.

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The Role of Chondrocyte Hypertrophy and Senescence in Osteoarthritis Initiation and Progression

Cited by 210 publications

References 105 publications

The Role of Autophagy in Osteoarthritis

The Role of Autophagy in Osteoarthritis

LncRNA MEG3 Protects Chondrocytes From IL-1β-Induced Inflammation via Regulating miR-9-5p/KLF4 Axis

The Role of Fibrosis in Osteoarthritis Progression

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