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Evidence for a protective role for adiponectin in osteoarthritis

机译:脂联素在骨关节炎中起保护作用的证据

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Obesity has been associated with an increased risk of osteoarthritis (OA). However, the mechanism by which obesity contributes to OA remains uncertain. Adiponectin, an adipocyte-derived hormone, has shown anti-diabetic and anti-atherogenic properties. In the present study, we aimed to investigate the potential role of adiponectin in OA disease. We demonstrated that adiponectin was present in OA synovial fluid (SF) and its expression level was almost 100-fold decrease compared with that in OA plasma. FPLC and ELISA studies revealed the distribution and abundance of the adiponectin complexes in plasma and SF from patients with OA. The percentage of high molecular weight (HMW) per total adiponectin in OA SF was lower than in OA plasma, while that of the hexamer form was similar and the trimer form was higher. The expression levels of adiponectin receptors AdipoR1 and AdipoR2 were examined in human OA tissues by RT-PCR. AdipoR1 was abundantly expressed in cartilage, bone and synovial tissues, whereas AdipoR2 was rarely detected. Finally, the effects of adiponectin on primary chondrocyte functions were studied by using antibody-based protein array and RT-PCR. The patterns of mRNA expression and protein production strongly indicate that adiponectin is involved in the modulation of cartilage destruction in chondrocytes by up-regulating TIMP-2 and down-regulating IL-1 beta-induced MMP-13. Together these findings clearly indicate that the adiponectin may act as a protective role in the progression of OA, and this also provide new thinking on the relationship between obesity and OA. (c) 2006 Elsevier B.V. All rights reserved.
机译:肥胖与骨关节炎(OA)的风险增加有关。然而,肥胖促成OA的机制仍不确定。脂联素,一种来自脂肪细胞的激素,已显示出抗糖尿病和抗动脉粥样硬化的特性。在本研究中,我们旨在调查脂联素在OA疾病中的潜在作用。我们证明脂联素存在于OA滑液(SF)中,其表达水平与OA血浆相比下降了近100倍。 FPLC和ELISA研究揭示了OA患者血浆和SF中脂联素复合物的分布和丰度。 OA SF中每总脂连蛋白的高分子量(HMW)百分比低于OA血浆中的百分比,而六聚体形式的百分比相似,而三聚体形式的百分比更高。通过RT-PCR检测脂联素受体AdipoR1和AdipoR2在人OA组织中的表达水平。 AdipoR1在软骨,骨骼和滑膜组织中大量表达,而很少检测到AdipoR2。最后,通过基于抗体的蛋白质阵列和RT-PCR研究了脂联素对原代软骨细胞功能的影响。 mRNA表达和蛋白质产生的模式强烈表明,脂联素通过上调TIMP-2和下调IL-1β诱导的MMP-13参与软骨细胞软骨破坏的调节。这些发现共同表明脂联素可能在OA的发展中起保护作用,这也为肥胖与OA之间的关系提供了新的思路。 (c)2006 Elsevier B.V.保留所有权利。

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