کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2167058 | 1092303 | 2014 | 5 صفحه PDF | دانلود رایگان |
• CD14+ cells express prolactin receptor.
• Prolactin receptors are increased in rheumatoid arthritis patients.
• Activating the prolactin receptor induces release of TNF-α from CD14+ cells.
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.
Journal: Cellular Immunology - Volume 290, Issue 1, July 2014, Pages 164–168