Ageing and Osteoarthritis

Sacitharan, Pradeep Kumar

doi:10.1007/978-981-13-3681-2_6

Cited by 242 publications

(179 citation statements)

References 197 publications

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“…Osteoarthritis (OA) is a common disease occurred in the elder that seriously affects the quality of life among elderly people and costs huge medical expenses [1]. With the ageing population gradually increased, the morbidity of OA is increased accordingly [2]. Until now, no such drug has shown efficacy at slowing or reversing joint damage during OA progression in humans.…”

Section: Introductionmentioning

confidence: 99%

Silence of lncRNA MIAT protects ATDC5 cells against lipopolysaccharides challenge via up-regulating miR-132

Song

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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The over-expanding role of lncRNA myocardial infarction associated transcript (MIAT) in various human diseases has been recently revealed. This study attempted to see the role of MIAT in a cell model of osteoarthritis (OA). ATDC5 cells were subjected to lipopolysaccharides (LPS) to mimic a cell model of OA. The effects of MIAT on the model were tested by performing CCK-8 assay, flow cytometry, qRT-PCR, western blot and ELISA. The downstream miRNA and signalling pathways were studied by utilizing qRT-PCR and western blot. Transfection of ATDC5 cells with the shRNA specific against MIAT significantly attenuated LPS-evoked apoptosis and cytokines release. At the meantime, the viability loss and the cleavage of caspases were ameliorated as well. MIAT overexpressed lead to the opposite result. Further, miR-132 was found to be negatively regulated by MIAT. The protective effects of MIAT silence were flattened when miR-132 expression was suppressed. Besides that the inhibitory effects of MIAT silence on LPS-evoked NF-jB and JNK activation were eliminated by miR-132 silence. This study illustrated that silence of MIAT protected ATDC5 cells against LPS challenge. The chondroprotective effects of MIAT silence may be via up-regulation of miR-132 and inhibition of NF-jB and JNK pathways.

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Section: Introductionmentioning

confidence: 99%

Silence of lncRNA MIAT protects ATDC5 cells against lipopolysaccharides challenge via up-regulating miR-132

Song

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…OA is a degenerative disease of the synovial joints, which is characterized by synovium inflammation, progressive degradation of cartilage and the associated extracellular matrix, osteophyte formation and subchondral bone sclerosis [2]. OA is the most common reason of synovial joint pain and dysfunction in the older adults [3]. The disease progression of OA affects not only articular cartilage, but also the entire joint, including subchondral bone, articular capsule, synovial membrane and surrounding muscles.…”

Section: Introductionmentioning

confidence: 99%

The Role of Autophagy and Mitophagy in Bone Metabolic Disorders

et al. 2020

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Bone metabolic disorders include osteolysis, osteoporosis, osteoarthritis and rheumatoid arthritis. Osteoblasts and osteoclasts are two major types of cells in bone constituting homeostasis. The imbalance between bone formation by osteoblasts and bone resorption by osteoclasts has been shown to have a direct contribution to the onset of these diseases. Recent evidence indicates that autophagy and mitophagy, the selective autophagy of mitochondria, may play a vital role in regulating the proliferation, differentiation and function of osteoblasts and osteoclasts. Several signaling pathways, including PINK1/Parkin, SIRT1, MAPK8/FOXO3, Beclin-1/BECN1, p62/SQSTM1, and mTOR pathways, have been implied in the regulation of autophagy and mitophagy in these cells. Here we review the current progress about the regulation of autophagy and mitophagy in osteoblasts and osteoclasts in these bone metabolic disorders, as well as the molecular signaling activated or deactivated during this process. Together, we hope to draw attention to the role of autophagy and mitophagy in bone metabolic disorders, and their potential as a new target for the treatment of bone metabolic diseases and the requirements of further mechanism studies.

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“…Osteoarthritis (OA) is a complex disease characterized by progressive cartilage loss, underlying bone remodeling, associated inflammation and subsequent joint failure 1 . Aging is the critical rick factor for OA, while the mechanisms linking age and OA have not been completely understood 2 . Chondrocytes, as the only resident cells in cartilage, can maintain the structure and function of cartilage by synthetizing extracellular matrix molecules 3 .…”

Section: Introductionmentioning

confidence: 99%

“…Chondrocytes, as the only resident cells in cartilage, can maintain the structure and function of cartilage by synthetizing extracellular matrix molecules 3 . However, physicochemical irritation, such as abnormal mechanical loading or proinflammatory cytokines, may damage chondrocytes and induce inflammatory and catabolic responses, which may exacerbate cartilage matrix degradation and accelerate OA progression 2,4 .…”

Section: Introductionmentioning

confidence: 99%

MFN2 contributes to metabolic disorders and inflammation in the aging of rat chondrocytes and osteoarthritis

et al. 2020

Osteoarthritis and Cartilage

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Objective: Metabolic disorders and inflammation of chondrocytes are major pathological changes in aging cells and osteoarthritis (OA). Recent studies demonstrated age-related mitochondrial dysfunction may be a key contributing factor in the development of OA. Mitofusin 2 (MFN2) is a key regulator of mitochondrial fusion, cell metabolism, autophagy and apoptosis. This study was performed to ascertain whether MFN2 was involved in the aging of chondrocytes and OA. Methods: Metabolic measurements were taken in rat chondrocytes between different ages (3-week, 5month, 12-month). MFN2 activity was detected in both human and rat chondrocytes during aging and OA. Then, knockdown of MFN2 with small interfering RNA (siRNA) was performed to confirm whether MFN2 contributes to metabolic changes. Lentiviruses were used to establish MFN2-overexpression/ knockdown OA models both in vivo and in vitro to confirm whether MFN2 contributes to OA progress. Further, regulatory mechanism of MFN2 was assessed and interaction between MFN2 and PARKIN was performed. Results: A metabolic shift to mitochondrial respiration was confirmed in rat chondrocytes during aging. MFN2 expression was elevated in both human and rat chondrocytes during aging and OA. Knockdown of MFN2 with siRNA reversed the age-related metabolic changes in rat chondrocytes. Overexpression of MFN2 exacerbated inflammation and OA progress, while knockdown of MFN2 ameliorated inflammation and OA progress. Further, MFN2 could be ubiquitinated by PARKIN, declined PARKIN expression during aging and OA might result in elevated MFN2 expression. Conclusions: Elevated MFN2 contributes to metabolic changes and inflammation during aging of rat chondrocytes and osteoarthritis.

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Ageing and Osteoarthritis

Cited by 242 publications

References 197 publications

Silence of lncRNA MIAT protects ATDC5 cells against lipopolysaccharides challenge via up-regulating miR-132

Silence of lncRNA MIAT protects ATDC5 cells against lipopolysaccharides challenge via up-regulating miR-132

The Role of Autophagy and Mitophagy in Bone Metabolic Disorders

MFN2 contributes to metabolic disorders and inflammation in the aging of rat chondrocytes and osteoarthritis

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