A longitudinal analysis of serum cytokines in the Hartley guinea pig model of osteoarthritis

Huebner, Janet L.; Seifer, D.R.; Kraus, Virginia B.

doi:10.1016/j.joca.2006.10.014

Cited by 26 publications

(20 citation statements)

References 12 publications

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“…It has been con rmed that the levels of pro-in ammatory cytokines, such as TNF-and IL-1b, increase sharply during the early stages of OA progression. Animal and in vitro studies have con rmed that the in ammatory cytokine TNF-can induce bone resorption and enhance cartilage degradation in OA [41,42]. In our study, we found higher immunohistochemical and mRNA expression of TNF-, which can stimulate the production of other cytokines, such as IL-6, prostaglandin, and MMP [41] as well as decrease type II collagen and proteoglycan levels [43].…”

Section: Discussionsupporting

confidence: 63%

Early Patellofemoral Articular Cartilage Degeneration in a Rat Model of Patellar Instability is Associated with Activation of the NF-κB Signaling Pathway

Lin

Dai

Yang

et al. 2020

Preprint

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Background: Patellar instability (PI) often increases the possibility of lateral patellar dislocation and early osteoarthritis. The molecular mechanism of early articular cartilage degeneration during patellofemoral osteoarthritis (PFOA) still requires further investigation. However, it is known that the NF-κB signaling pathway plays an important role in articular cartilage degeneration. The aim of this study was to investigate the relationship between the NF-κB signaling pathway and patellofemoral joint cartilage degeneration. Methods: We established a rat model of PI-induced PFOA. Female 4-week-old Sprague-Dawley rats (n=120) were randomly divided into two groups: the PI (n=60) and control group (n=60). The distal femurs of the PI and control group were isolated and compared 4, 8, and 12 weeks after surgery. The morphological structure of the trochlear cartilage and subchondral bone were evaluated by micro-computed tomography and histology. The expression of NF-κB, matrix metalloproteinase (MMP)-13, collagen X, and TNF-ɑ were evaluated by immunohistochemistry and quantitative polymerase chain reaction. Results: In the PI group, subchondral bone loss and cartilage degeneration were found 4 weeks after surgery. Compared with the control group, the protein and mRNA expression of NF-κB and TNF-ɑ were significantly increased 4, 8, and 12 weeks after surgery in the PI group. In addition, the markers of cartilage degeneration MMP-13 and collagen X were more highly expressed in the PI group compared with the control group at different time points after surgery.Conclusions: This study has demonstrated that early patellofemoral joint cartilage degeneration can be caused by PI in growing rats, accompanied by significant subchondral bone loss and cartilage degeneration. In addition, the degeneration of articular cartilage may be associated with the activation of the NF-κB signaling pathway and can deteriorate with time as a result of PI.

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Section: Discussionsupporting

confidence: 63%

Early Patellofemoral Articular Cartilage Degeneration in a Rat Model of Patellar Instability is Associated with Activation of the NF-κB Signaling Pathway

Lin

Dai

Yang

et al. 2020

Preprint

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“… 45 , 46 In Hartley guinea pig model of OA, IL-6 levels in serum were positively correlated with histological score of OA, which was independent of age or weight. 47 Another report by Tonchera et al 48 concluded that serum levels of IL-6 were significantly higher in patients with active OA compared with healthy subjects. Furthermore, there is a direct correlation in IL-6 expression level and clinical outcome of rheumatoid arthritis, and blocking of IL-6 function has emerged a new therapeutic strategy for RA and related inflammatory disease.…”

Section: Discussionmentioning

confidence: 97%

miR-139 modulates MCPIP1/IL-6 expression and induces apoptosis in human OA chondrocytes

Makki

Haqqi

2015

Exp Mol Med

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IL-6 is an inflammatory cytokine and its overexpression plays an important role in osteoarthritis (OA) pathogenesis. Expression of IL-6 is regulated post-transcriptionally by MCPIP1. The 3′ untranslated region (UTR) of MCPIP1 mRNA harbors a miR-139 ‘seed sequence', therefore we examined the post-transcriptional regulation of MCPIP1 by miR-139 and its impact on IL-6 expression in OA chondrocytes. Expression of miR-139 was found to be high in the damaged portion of the OA cartilage compared with unaffected cartilage from the same patient and was also induced by IL-1β in OA chondrocytes. Inhibition of miR-139 decreased the expression of IL-6 mRNA by 38% and of secreted IL-6 protein by 40%. However, overexpression of miR-139 increased the expression of IL-6 mRNA by 36% and of secreted IL-6 protein by 56%. These data correlated with altered expression profile of MCPIP1 in transfected chondrocytes. Studies with a luciferase reporter construct confirmed the interactions of miR-139 with the ‘seed sequence' located in the 3′ UTR of MCPIP mRNA. Furthermore, miR-139 overexpression increased the catabolic gene expression but expression of anabolic markers remained unchanged. Overexpression of miR-139 also induced apoptosis in OA chondrocytes. Importantly, we also discovered that IL-6 is a potent inducer of miR-139 expression in OA chondrocytes. These findings indicate that miR-139 functions as a post-transcriptional regulator of MCPIP1 expression and enhances IL-6 expression, which further upregulates miR-139 expression in OA chondrocytes. These results support our hypothesis that miR-139-mediated downregulation of MCPIP1 promotes IL-6 expression in OA. Therefore, targeting miR-139 could be therapeutically beneficial in the management of OA.

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“…48 Significant positive correlations were found between the SDF-1, GAG, and C2C synovial fluid concentrations and the Mankin score. Huebner et al 46,49 showed that the Hartley strain exemplified a serum/chemokine profile indicative of a pro-inflammatory state compared with Strain 13. Among the cytokines and chemokines elevated in the Hartley strain, they found IL-6, IL-17, IL-8, and TNF-α.…”

Section: Guinea Pigsmentioning

confidence: 99%

Review of Soluble Biomarkers of Osteoarthritis: Lessons From Animal Models

et al. 2016

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Objective. Osteoarthritis (OA) is one of the leading causes of disability within the adult population. Currently, its diagnosis is mainly based on clinical examination and standard radiography. To date, there is no way to detect the disease at a molecular level, before the appearance of structural changes and symptoms. So an attractive alternative for monitoring OA is the measurement of biochemical markers in blood, urine, or synovial fluid, which could reflect metabolic changes in joint tissue and therefore disease onset and progression. Animal models are relevant to investigate the early stage of OA and metabolic changes occurring in joint tissues. The goal of this narrative review is to summarize the scientific data available in the literature on soluble biomarkers in animal models of OA. Design. A literature search was conducted using the PubMed/ Medline and Scopus databases between February 1995 and December 2015. All original articles, systematic and narrative reviews published in French or in English were considered. Results. We summarized the data of 69 studies and proposed a classification scheme for OA biomarkers in animal studies, largely inspired by the BIPEDS classification. Conclusions. Studies about biomarkers and animal models indicate that some markers could be valuable to monitor OA progression and assess therapeutic response in some animal models.

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A longitudinal analysis of serum cytokines in the Hartley guinea pig model of osteoarthritis

Cited by 26 publications

References 12 publications

Early Patellofemoral Articular Cartilage Degeneration in a Rat Model of Patellar Instability is Associated with Activation of the NF-κB Signaling Pathway

Early Patellofemoral Articular Cartilage Degeneration in a Rat Model of Patellar Instability is Associated with Activation of the NF-κB Signaling Pathway

miR-139 modulates MCPIP1/IL-6 expression and induces apoptosis in human OA chondrocytes

Review of Soluble Biomarkers of Osteoarthritis: Lessons From Animal Models

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