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

Chun Tang; Yun Li; Xiaojun Lin; Jinghua Ye; Weinian Li; Zhixiang He; Fangfei Li; Xiaoyan Cai

doi:10.1016/j.cellimm.2014.06.005

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

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

Authors

Chun Tang¹, Yun Li², Xiaojun Lin¹, Jinghua Ye¹, Weinian Li¹, Zhixiang He¹, Fangfei Li¹, Xiaoyan Cai³

Affiliations

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

PMID: 24997655
DOI: 10.1016/j.cellimm.2014.06.005

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.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Arthritis, Rheumatoid / immunology*
Flavonoids / pharmacology
Gene Expression Regulation / immunology
Gene Silencing
Humans
Lipopolysaccharide Receptors / biosynthesis
MAP Kinase Signaling System / immunology
Monocytes / immunology*
Prolactin / metabolism
Protein Kinase Inhibitors / pharmacology
Receptors, Prolactin / genetics*
Receptors, Prolactin / immunology
Tumor Necrosis Factor-alpha / biosynthesis*
Tumor Necrosis Factor-alpha / immunology
p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors*
p38 Mitogen-Activated Protein Kinases / immunology

Substances

Flavonoids
Lipopolysaccharide Receptors
Protein Kinase Inhibitors
Receptors, Prolactin
Tumor Necrosis Factor-alpha
Prolactin
p38 Mitogen-Activated Protein Kinases
2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one