Cytokine induction of prolactin receptors mediates prolactin inhibition of nitric oxide synthesis in pulmonary fibroblasts

FEBS Letters

Cross, Carroll E.²  Corbacho, Ana M.¹  Eiserich, Jason P.²  Nava, Gabriel¹  Martı́nez de la Escalera, Gonzalo¹  Clapp, Carmen¹  Macotela, Yazmin¹ 

[1]Instituto de Neurobiologı́a, Universidad Nacional Autónoma de México, Campus UNAM-Juriquilla, Apartado Postal 1-1141, Juriquilla-Querétaro, Qro. 76001, Mexico

[2]Divisions of Pulmonary and Critical Care Medicine and nephrology, Department of Internal Medicine, University of California at Davis, Davis, CA 95616, USA

关键词: Prolactin;    Prolactin receptor;    Nitric oxide;    iNOS;    Pro-inflammatory cytokine;    STAT-5b;    IRF-1;    PRL;    prolactin;    iNOS;    inducible nitric oxide synthase;    IL-1β;    interleukin 1β;    IFNγ;    interferon γ;    TNFα;    tumor necrosis factor α;    STAT-5b;    signal transducer and activator of transcription 5b;    IRF-1;    interferon regulatory factor 1;   

DOI  :  10.1016/S0014-5793(03)00499-X

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Prolactin (PRL) has been implicated as a modulator of immune function, and some of its actions may be linked to NO synthesis. Because NO acts as a mediator of inflammation, we speculated that an inflammatory milieu could unmask pathways by which PRL could affect NO synthesis. Here, we show that pro-inflammatory cytokines induce the expression of PRL receptors in pulmonary fibroblasts, allowing PRL to inhibit cytokine-induced NO production and the expression of the inducible nitric oxide synthase (iNOS). Inhibition of iNOS expression by PRL correlates with the phosphorylation of STAT-5b (signal transducer and activator of transcription 5b) and the suppression of expression of IRF-1 (interferon regulatory factor 1), a transcription factor for iNOS. These results reveal previously unrecognized mechanisms by which PRL and PRL receptors may play significant modulatory roles during immune–inflammatory processes.

【 授权许可】

Unknown