circPhc3 sponging microRNA‑93‑3p is involved in the regulation of chondrocyte function by mechanical instability in osteoarthritis

Wang, Zhiyuan; Rao, Zhi-Ren; Wang, Xin; Jiang, Chao; Yang, Yi

doi:10.3892/ijmm.2021.5061

Cited by 6 publications

(2 citation statements)

References 43 publications

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“…For example, circSEC24A is upregulated in OA cartilage tissues and chondrocytes. This upregulation aggravates IL-1β-induced injury by downregulating IL-1β and reducing miR-142-5p in IL-1β-stimulated chondrocytes [ 138 ]. CircSCAPER promotes IL-1β-induced ECM degradation, proliferation arrest, and apoptosis enhancement in human chondrocytes by regulating the miR-140-3p/EZH2 axis [ 139 ].…”

Section: Ncrnas Involved In Cartilage Homeostasis and Oamentioning

confidence: 99%

Cartilage Homeostasis and Osteoarthritis

Fujii

Liu

Yagasaki

et al. 2022

IJMS

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Healthy limb joints are important for maintaining health and attaining longevity. Endochondral ossification (the replacement of cartilage with bone, occurring during skeletal development) is essential for bone formation, especially in long-axis bones. In contrast to endochondral ossification, chondrocyte populations in articular cartilage persist and maintain joint tissue into adulthood. Articular cartilage, a connective tissue consisting of chondrocytes and their surrounding extracellular matrices, plays an essential role in the mechanical cushioning of joints in postnatal locomotion. Osteoarthritis (OA) pathology relates to disruptions in the balance between anabolic and catabolic signals, that is, the loss of chondrocyte homeostasis due to aging or overuse of cartilages. The onset of OA increases with age, shortening a person’s healthy life expectancy. Although many people with OA experience pain, the mainstay of treatment is symptomatic therapy, and no fundamental treatment has yet been established. To establish regenerative or preventative therapies for cartilage diseases, further understanding of the mechanisms of cartilage development, morphosis, and homeostasis is required. In this review, we describe the general development of cartilage and OA pathology, followed by a discussion on anabolic and catabolic signals in cartilage homeostasis, mainly microRNAs.

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Section: Ncrnas Involved In Cartilage Homeostasis and Oamentioning

confidence: 99%

Cartilage Homeostasis and Osteoarthritis

Fujii

Liu

Yagasaki

et al. 2022

IJMS

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“…Chondrocytes at 70% confluence were transfected using Lipofectamine 3000 reagent (Invitrogen). e transfection efficiency was detected 24 h after transfection and all functional experiments were performed 48 h after transfection [18].…”

Section: Cell Transfection Circmelk or Myd88 Overexpression Vector Wa...mentioning

confidence: 99%

Circular RNA MELK Promotes Chondrocyte Apoptosis and Inhibits Autophagy in Osteoarthritis by Regulating MYD88/NF-κB Signaling Axis through MicroRNA-497-5p

Zhang

Huang

et al. 2022

Contrast Media & Molecular Imaging

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Osteoarthritis (OA) is a rheumatic disease and its pathogenesis involves the dysregulation of noncoding RNAs. Therefore, the regulatory mechanism of circular RNA MELK (circMELK) was specified in this work. OA human cartilage tissue was collected, and circMELK, miR-497-5p, and myeloid differentiation factor 88 (MYD88) expression were examined. Human chondrocytes were stimulated with interleukin- (IL-) 1β and interfered with vectors altering circMELK, miR-497-5p, and MyD88 expression to observe their effects on cell viability, cell cycle and apoptosis, autophagy, and inflammation. The binding relationship between RNAs was verified. The data presented that OA cartilage tissues presented raised circMELK and MYD88 and inhibited miR-497-5p expression. IL-1β suppressed cell viability, prevented cell cycle, and induced apoptosis, autophagy, and inflammation of chondrocytes. Functionally, IL-1β-induced changes of chondrocytes could be attenuated by suppressing circMELK or overexpressing miR-497-5p. circMELK acted as a sponge of miR-497-5p while miR-497-5p was a regulator of MYD88. MYD88 restricted the effect of overexpressing miR-497-5p on IL-1β-stimulated chondrocytes. MYD88 triggered nuclear factor-kappaB (NF-κB) pathway activation. Shortly, CircMELK promotes chondrocyte apoptosis and inhibits autophagy in OA by regulating MYD88/NF-κB signaling axis through miR-497-5p. Our study proposes a new molecular mechanism for the development of OA.

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