Gross Jean-Baptiste, Guillaume Cecile, Gegout-Pottie Pascale, Reboul Pascal, Jouzeau Jean-Yves, Mainard Didier, Presle Nathalie
UMR 7365 CNRS-Université de Lorraine, Faculté de Medecine, Vandoeuvre-les-Nancy, France.
Clin Exp Rheumatol. 2017 Jan-Feb;35(1):53-60. Epub 2016 Nov 13.
Based on a novel approach suggesting a role of adipose tissue in osteoarthritis (OA), we aimed to determine whether the infrapatellar fat pad (IFP) may affect joint cell functions through adipokines.
The conditioned media of IFP and subcutaneous adipose tissue from OA patients were used to determine the production of leptin and adiponectin, and to stimulate chondrocytes and fibroblast-like synoviocytes (FLS). Blocking experiments were carried out to evaluate the contribution of adipokines to IFP effects. The gene expression of inflammatory and degradative proteins, growth factors and components of the extracellular matrix, and the production of inflammatory mediators and metalloproteases were determined to evaluate cell response to fat-conditioned media.
IFP releases elevated amounts of leptin and adiponectin independently of the body mass index and the gender. The conditioned media from IFP strongly induce the expression of inflammatory genes in both articular cells and the expression of degradative genes in chondrocytes, but remain ineffective in regulating the expression of aggrecan, type 2 collagen or growth factors. Blocking leptin or adiponectin does not change the cell response to IFP. A great variability between patients is found when compared the inflammatory activity of paired samples of IFP and subcutaneous adipose tissue.
IFP may trigger both cartilage destruction and inflammation of the synovium, but not through leptin or adiponectin. The data suggest also that IFP may have specific inflammatory phenotypic features independent from the general phenotype found in obesity.
基于一种表明脂肪组织在骨关节炎（OA）中起作用的新方法，我们旨在确定髌下脂肪垫（IFP）是否可能通过脂肪因子影响关节细胞功能。
使用OA患者的IFP和皮下脂肪组织的条件培养基来测定瘦素和脂联素的产生，并刺激软骨细胞和成纤维样滑膜细胞（FLS）。进行阻断实验以评估脂肪因子对IFP作用的贡献。测定炎症和降解蛋白、生长因子和细胞外基质成分的基因表达，以及炎症介质和金属蛋白酶的产生，以评估细胞对脂肪条件培养基的反应。
IFP释放的瘦素和脂联素量升高，与体重指数和性别无关。IFP的条件培养基强烈诱导关节细胞中炎症基因的表达以及软骨细胞中降解基因的表达，但在调节聚集蛋白聚糖、II型胶原蛋白或生长因子的表达方面仍然无效。阻断瘦素或脂联素不会改变细胞对IFP的反应。比较IFP和皮下脂肪组织的配对样本的炎症活性时，发现患者之间存在很大差异。
IFP可能引发软骨破坏和滑膜炎症，但不是通过瘦素或脂联素。数据还表明，IFP可能具有独立于肥胖中发现的一般表型的特定炎症表型特征。
