Correlation between Gene Expression and Osteoarthritis Progression in Human

Zhong, Leilei; Huang, Xiaobin; Karperien, Marcel; Post, Janine N.

doi:10.3390/ijms17071126

Cited by 89 publications

(83 citation statements)

References 55 publications

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“…The present study revealed a significant difference in IHH expression in the middle layer of the OAG compared with those in the CG and COAG. Similar results were reported by Zhong et al [54], who related the progression of OA to the expression of IHH. Van der Kraan and Van den Berg [55] suggested a correlation between IHH expression and the progression of OA in animal models, due to protease-mediated effects on the progression of OA.…”

Section: Plos Onesupporting

confidence: 90%

Evaluation of the articular cartilage in the knees of rats with induced arthritis treated with curcumin

2020

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This study was designed to evaluate the anti-inflammatory effects of a curcumin treatment on the knee of rats with induced osteoarthritis. Fifteen adult rats were used and divided in three groups: the osteoarthritis group (OAG), control group (CG-without induction of osteoarthritis), and curcumin-treated osteoarthritis group (COAG). Osteoarthritis was induced in the right knee of rats in the OAG and COAG by administering an intra-articular injection of 1 mg of zymosan. Fourteen days after induction, 50 mg/kg curcumin was administered by gavage daily for 60 days to the COAG. After the treatment period, rats from all groups were euthanized. Medial femoral condyles were collected for light microscopy and immunohistochemical staining. The expression of SOX-5, IHH, MMP-8, MMP-13, and collagen 2 (Col2) was analyzed. The COAG exhibited an increase in the number of chondrocytes in the surface and middle layers compared with that of the OAG and CG, respectively. The COAG also showed a decrease in the thicknesses of the middle and deep layers compared with those of the OAG, and an increase in Col2 expression was observed in all articular layers (surface, middle, and deep) in the COAG compared with that in the OAG. SOX-5 expression was increased in the surface and deep layers of the COAG compared with those in the OAG and CG. Based on the results of this study, the curcumin treatment appeared to exert a protective effect on cartilage, as it did not result in an increase in cartilage thickness or in MMP-8 and MMP-13 expression but led to increased IHH, Col2, and SOX-5 expression and the number of chondrocytes.

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Section: Plos Onesupporting

confidence: 90%

Evaluation of the articular cartilage in the knees of rats with induced arthritis treated with curcumin

2020

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“…Then the slides were stained for glycosaminoglycans (GAG) with a 0.5% w/v solution of Alcian blue (pH = 1, adjusted with HCl) for 30 min, or stained for sulfated GAG with a 0.1% solution of Safranin O for 5 min (Sigma Aldrich). Images were taken using a Nanozoomer (Iwata City, Japan) …”

Section: Methodsmentioning

confidence: 99%

Different response of human chondrocytes from healthy looking areas and damaged regions to IL1β stimulation under different oxygen tension

Huang

Zhong

Hendriks

et al. 2018

Journal Orthopaedic Research

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Due to its avascular nature, articular cartilage is relatively hypoxic. The aim of this study was to elucidate the functional changes of macroscopically healthy looking areas chondrocytes (MHC) and macroscopically damaged regions chondrocytes (MDC) at a cellular level in response to the inflammatory cytokine IL1β under different oxygen tension levels. In this study, two‐dimensional (2‐D) expanded MHC and MDC were redifferentiated in 3‐D pellet cultures in chondrogenic differentiation medium, supplemented with or without IL1β at conventional culture (normoxia) or 2.5% O2 (hypoxia) for 3 weeks. qPCR, immunohistochemistry and ELISA were used to detect the expression of anabolic and catabolic gene expression. Alcian blue/Safranin O staining and GAG assay were used to measure cartilage matrix production. Cell proliferation and apoptosis were assessed by EdU staining and TUNEL assay, respectively. The results showed that hypoxia enhanced matrix production in both MHC and MDC and this effect was stronger on MDC. Under normoxia, MHC showed higher expression of cartilage markers and lower catabolic genes expression than MDC. Interestingly, hypoxia diminished the difference between MHC and MDC. IL1β potently induced MMPs expression regardless of cell population and oxygen tension. The fold induction of these MMPs in hypoxia was however much higher than in normoxia. In addition, hypoxia promoted the expression of HIF1α and HIF2α in MHC, while it only enhanced HIF1α expression but decreased the HIF2α expression in MDC. We concluded that hypoxia stimulated the redifferentiation of cultured chondrocytes, particularly in MDC derived from macroscopically diseased cartilage. Oxygen tension may profoundly and differentially influence inflammation‐associated cartilage injury and diseases by regulating the expression of HIF1α and HIF2α. © 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 9999:XX–XX, 2018.

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“…Studies in human OA cartilage are naturally variable, and the evaluation of the mRNA and protein levels of transcriptional regulators is influenced by disease stage and proximity to cartilage lesions. For instance, while the expression levels of SOX9 and COL2A1 do not always correlate in OA disease, some studies have reported that SOX9 , COL2A1 , and ACAN mRNA levels decrease with increasing OA severity, and that the increased expression of SOX9 in early disease correlates with reduced production of ADAMTSs and increased expression of COL2A1, COMP, and ACAN . These apparent discrepancies can be partly explained by the complex contribution of other factors like ELF3, with antianabolic and procatabolic functions in chondrocytes and with the ability to disrupt the SOX9–CBP/p300 interaction.…”

Section: Transcriptional Network Driving Articular Chondrocyte Hypermentioning

confidence: 99%

Phenotypic instability of chondrocytes in osteoarthritis: on a path to hypertrophy

Singh

Marcu

Goldring

et al. 2018

Annals of the New York Academy of Sciences

114

139

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Articular chondrocytes are quiescent, fully differentiated cells responsible for the homeostasis of adult articular cartilage by maintaining cellular survival functions and the fine-tuned balance between anabolic and catabolic functions. This balance requires phenotypic stability that is lost in osteoarthritis (OA), a disease that affects and involves all joint tissues and especially impacts articular cartilage structural integrity. In OA, articular chondrocytes respond to the accumulation of injurious biochemical and biomechanical insults by shifting toward a degradative and hypertrophy-like state, involving abnormal matrix production and increased aggrecanase and collagenase activities. Hypertrophy is a necessary, transient developmental stage in growth plate chondrocytes that culminates in bone formation; in OA, however, chondrocyte hypertrophy is catastrophic and it is believed to initiate and perpetuate a cascade of events that ultimately result in permanent cartilage damage. Emphasizing changes in DNA methylation status and alterations in NF-κB signaling in OA, this review summarizes the data from the literature highlighting the loss of phenotypic stability and the hypertrophic differentiation of OA chondrocytes as central contributing factors to OA pathogenesis.

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Correlation between Gene Expression and Osteoarthritis Progression in Human

Cited by 89 publications

References 55 publications

Evaluation of the articular cartilage in the knees of rats with induced arthritis treated with curcumin

Evaluation of the articular cartilage in the knees of rats with induced arthritis treated with curcumin

Different response of human chondrocytes from healthy looking areas and damaged regions to IL1β stimulation under different oxygen tension

Phenotypic instability of chondrocytes in osteoarthritis: on a path to hypertrophy

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