Experimental Osteoarthritis Models in Mice

Lorenz, Julia; Grässel, Susanne

doi:10.1007/978-1-4939-1215-5_23

Cited by 102 publications

(86 citation statements)

References 36 publications

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“…First, medial radial displacement (MRD) of the medial meniscus is considered a signature feature of knee OA. The cause of the protrusion is unknown, but MRD may play a hitherto unappreciated role in the pathogenesis of OA due to its close relationship with the medial collateral ligament 14. Bevers et al 15 were the first to study the interobserver reliability reporting a moderate κ for two observers.…”

Section: Discussionmentioning

confidence: 99%

An OMERACT reliability exercise of inflammatory and structural abnormalities in patients with knee osteoarthritis using ultrasound assessment

Bruyn¹,

Naredo

Damjanov

et al. 2015

Ann Rheum Dis

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Objective To assess whether ultrasonography (US) is reliable for the evaluation of inflammatory and structural abnormalities in patients with knee osteoarthritis (OA). Methods Thirteen patients with early knee OA were examined by 11 experienced sonographers during 2 days. Dichotomous and semiquantitative scoring was performed on synovitis characteristics in various aspects of the knee joint. Semiquantitative scoring was done of osteophytes at the medial and lateral femorotibial joint space or cartilage damage of the trochlea and on medial meniscal damage bilaterally. Intra-and interobserver reliability were computed by use of unweighted and weighted κ coefficients. Results Intra-and interobserver reliability scores were moderate to good for synovitis (mean κ 0.67 and 0.52, respectively) as well as moderate to good for the global synovitis (0.70 and 0.50, respectively). Mean intra-and interobserver reliability κ for cartilage damage, medial meniscal damage and osteophytes ranged from fair to good (0.55 and 0.34, 0.75 and 0.56, 0.73 and 0.60, respectively). Conclusions Using a standardised protocol, dichotomous and semiquantitative US scoring of pathological changes in knee OA can be reliable.

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Section: Discussionmentioning

confidence: 99%

An OMERACT reliability exercise of inflammatory and structural abnormalities in patients with knee osteoarthritis using ultrasound assessment

Bruyn¹,

Naredo

Damjanov

et al. 2015

Ann Rheum Dis

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“…The proteoglycan content of the articular cartilage was graded on Safranin-O-stained sections using OARSI histology scoring system as previously reported [12]. Moreover, the histological analyses of cartilage destruction were done as previously reported [13].…”

Section: Histopathologic and Quantificational Evaluation Of Oamentioning

confidence: 99%

Naringin Protects Against Cartilage Destruction in Osteoarthritis Through Repression of NF-κB Signaling Pathway

Zhao

Wang

et al. 2015

Inflammation

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Naringin was previously reported as a multifunctional agent. Recently, naringin was found to play a protective role in various inflammatory conditions. However, the role of naringin in cartilage degeneration and osteoarthritis (OA) progression is still unknown. TNF-α is reported to play a detrimental role in OA. Herein, primary murine chondrocytes were isolated and cultured with stimulation of TNF-α, in the presence or absence of naringin treatment. As a result, naringin attenuated TNF-α-mediated inflammation and catabolism in chondrocyte. Besides, surgically induced OA mice models were established. Cartilage degradation and OA severity were evaluated using Safranin-O staining, immunohistochemistry, and ELISA. Moreover, levels of inflammatory cytokines and catabolic markers in OA were analyzed. Oral administration of naringin alleviated degradation of cartilage matrix and protected against OA development in the surgically induced OA models. Furthermore, the protective function of naringin in cartilage and chondrocyte was possibly due to suppression of NF-κB signaling pathway. Collectively, this study presents naringin as a potential target for the treatment of joint degenerative diseases, including OA.

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“…Nine rats were randomly sacrificed at two days, four days, three weeks, four weeks, and six weeks subsequent to the surgery. The OA model was generated via surgery, according to a previous publication [25]. In short, the ligament cruciatum genu anterius or posterius, the meniscus medialis, and the ligamentum mediale of the posterior rat limbs were eliminated in order to bring about articular deformity, which led to the enhancement of damage to the articular face, as well as deterioration of joint cartilage.…”

Section: Surgical Stimulation Of Oamentioning

confidence: 99%

MiR-34a Enhances Chondrocyte Apoptosis, Senescence and Facilitates Development of Osteoarthritis by Targeting DLL1 and Regulating PI3K/AKT Pathway

Zhang

Hsu

Zhong

et al. 2018

Cell Physiol Biochem

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Background/Aims: Osteoarthritis (OA) is the prevalent degenerative disease caused by various factors. MicroRNAs are important regulators in the inflammation and immune response. The aim of this study was to investigate the effect of microRNA-34a (MiR-34a) on the death of chondrocytes, senescence, as well as its role in OA progression. Methods: A series of experiments involving CCK-8, flow cytometry, β-galactosidase staining and wound healing assays were conducted to determine the cellular capabilities of proliferation, cell apoptosis, senescence and the ability of cells to recover from injury, respectively. Binding sites between miR-34a and delta-like protein 1 (DLL1) were identified using a luciferase reporter system, whereas mRNA and protein expression of target genes was determined by RT-PCR and immunoblot, respectively. OA model was generated via surgery. Results: We found that miR-34a expression was increased in the cartilage of OA patients. In rat chondrocytes and chondrosarcoma cells, miR-34a transfections noticeably inhibited the expression of DLL1, triggered cell death and senescence, suppressed proliferation, and prevented scratch assay wound closure. However, transfection of a miR-34a inhibitor displayed adverse effects. Additionally, secretion and expression of factors associated with cartilage degeneration were altered via miR-34a. Moreover, miR-34a directly inhibits DLL1 mRNA. Furthermore, concentrations of DLL1, total PI3K, and p-AKT declined in chondrocytes that overexpress miR-34a. DLL1 overexpression elevated PI3K and p-AKT levels, and eliminated cell death triggered by a miR-34a mimic. In vivo, miR-34a remarkably inhibited miR-34a up-regulation, while enhanced the level of DLL1 expression. In the knee joints of surgery-induced OA rats, articular chondrocyte death and loss of cartilage were attenuated via miR-34a antagomir injection. Conclusions: These findings indicate that miR-34a contributes to chondrocyte death, causing OA progression through DLL1 and modulation of the PI3K/AKT pathway.

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Experimental Osteoarthritis Models in Mice

Cited by 102 publications

References 36 publications

An OMERACT reliability exercise of inflammatory and structural abnormalities in patients with knee osteoarthritis using ultrasound assessment

An OMERACT reliability exercise of inflammatory and structural abnormalities in patients with knee osteoarthritis using ultrasound assessment

Naringin Protects Against Cartilage Destruction in Osteoarthritis Through Repression of NF-κB Signaling Pathway

MiR-34a Enhances Chondrocyte Apoptosis, Senescence and Facilitates Development of Osteoarthritis by Targeting DLL1 and Regulating PI3K/AKT Pathway

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