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Prolactin increases tumor necrosis factor alpha expression in peripheral CD14 monocytes of patients with rheumatoid arthritis

机译:催乳素增加类风湿关节炎患者外周血CD14单核细胞中的肿瘤坏死因子α表达

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Tumor necrosis factor (TNF)-α is one of the major proinflammatory mediators of rheumatic arthritis (RA); the regulatory factors for TNF-α release is not fully understood. This study aims to investigate the role of prolactin receptor (PRLR) activation in regulating the expression and release of TNF-α from CD14+ monocytes. The results showed that the expression of PRLR was detectable in CD14+ monocytes of healthy subjects, which was markedly increased in RA patients. Exposure to PRL in the culture increased the expression and release of TNF-α from CD14+ monocytes, which was abolished by the PRLR gene silencing or blocking the mitogen activated protein (MAPK) pathway. We conclude that exposure to PRL increases TNF-α release from CD14+ monocytes of RA patients, which can be abolished by PRLR gene silencing or treating with MAPK inhibitor.
机译:肿瘤坏死因子(TNF)-α是风湿性关节炎(RA)的主要促炎介质之一。 TNF-α释放的调节因子尚未完全了解。这项研究旨在研究催乳素受体(PRLR)激活在调节CD14 +单核细胞中TNF-α的表达和释放中的作用。结果表明,在健康受试者的CD14 +单核细胞中可检测到PRLR的表达,而在RA患者中PRLR的表达显着增加。暴露于培养物中的PRL可增加CD14 +单核细胞中TNF-α的表达和释放,这可通过PRLR基因沉默或阻断有丝分裂原活化蛋白(MAPK)途径来消除。我们得出结论,暴露于PRL会增加RA患者CD14 +单核细胞从TNF-α释放,这可以通过PRLR基因沉默或用MAPK抑制剂治疗而消除。

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