Exploring the Crosstalk between Hydrostatic Pressure and Adipokines: An In Vitro Study on Human Osteoarthritic Chondrocytes
Autor: | Sara Tenti, Francesca Bellisai, Elena Rosanna Frati, Marcella Barbarino, Stefano Giannotti, Sara Cheleschi, Antonella Fioravanti |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
Male
medicine.medical_specialty obesity Hydrostatic pressure Type II collagen chondrocytes Adipose tissue Adipokine Apoptosis Matrix metalloproteinase medicine.disease_cause Catalysis Article lcsh:Chemistry Inorganic Chemistry Cyclin D1 Internal medicine visfatin Gene expression medicine Humans oxidative stress Physical and Theoretical Chemistry Nicotinamide Phosphoribosyltransferase lcsh:QH301-705.5 Molecular Biology adipokines Cells Cultured Spectroscopy Aged Wnt/β-catenin mechanical loading microRNA Chemistry Organic Chemistry General Medicine Middle Aged Computer Science Applications osteoarthritis Endocrinology lcsh:Biology (General) lcsh:QD1-999 Gene Expression Regulation hydrostatic pressure Female Adipokines Chondrocytes Hydrostatic pressure Mechanical loading MicroRNA Obesity Osteoarthritis Oxidative stress Visfatin Wnt/β-catenin Oxidative stress |
Zdroj: | International Journal of Molecular Sciences International Journal of Molecular Sciences, Vol 22, Iss 2745, p 2745 (2021) Volume 22 Issue 5 |
ISSN: | 1422-0067 |
Popis: | Obesity is a risk factor for osteoarthritis (OA) development and progression due to an altered biomechanical stress on cartilage and an increased release of inflammatory adipokines from adipose tissue. Evidence suggests an interplay between loading and adipokines in chondrocytes metabolism modulation. We investigated the role of loading, as hydrostatic pressure (HP), in regulating visfatin-induced effects in human OA chondrocytes. Chondrocytes were stimulated with visfatin (24 h) and exposed to high continuous HP (24 MPa, 3 h) in the presence of visfatin inhibitor (FK866, 4 h pre-incubation). Apoptosis and oxidative stress were detected by cytometry, B-cell lymphoma (BCL)2, metalloproteinases (MMPs), type II collagen (Col2a1), antioxidant enzymes, miRNA, cyclin D1 expressions by real-time PCR, and β-catenin protein by western blot. HP exposure or visfatin stimulus significantly induced apoptosis, superoxide anion production, and MMP-3, -13, antioxidant enzymes, and miRNA gene expression, while reducing Col2a1 and BCL2 mRNA. Both stimuli significantly reduced β-catenin protein and increased cyclin D1 gene expression. HP exposure exacerbated visfatin-induced effects, which were counteracted by FK866 pre-treatment. Our data underline the complex interplay between loading and visfatin in controlling chondrocytes’ metabolism, contributing to explaining the role of obesity in OA etiopathogenesis, and confirming the importance of controlling body weight for disease treatment. |
Databáze: | OpenAIRE |
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