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Cell Immunol. 2014 Jul;290(1):164-8. doi: 10.1016/j.cellimm.2014.06.005. Epub 2014 Jun 24.

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

Author information

  • 1Department of Rheumatology, Guangzhou First People's Hospital, Guangzhou Medical University, 1 Panfu Road, Guangzhou, China.
  • 2Department of Cardiothoracic Surgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
  • 3Department of Rheumatology, Guangzhou First People's Hospital, Guangzhou Medical University, 1 Panfu Road, Guangzhou, China. Electronic address: xycai@medmail.com.cn.

Abstract

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.

KEYWORDS:

Methylation specific PCR; Mitogen activated protein; Prolactin; Rheumatoid arthritis; Tumor necrosis factor-α

PMID:
24997655
DOI:
10.1016/j.cellimm.2014.06.005
[PubMed - indexed for MEDLINE]
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