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

被引：32

作者：

Corbacho, AM

Macotela, Y

Nava, G

Eiserich, JP

Cross, CE

de la Escalera, GM

Clapp, C

机构：

[1] Univ Nacl Autonoma Mexico, Inst Neurobiol, Juriquilla 76001, Queretaro, Mexico

[2] Univ Calif Davis, Dept Internal Med, Div Pulm & Crit Care Med, Dept Internal Med, Davis, CA 95616 USA

[3] Univ Calif Davis, Dept Internal Med, Div Nephrol, Dept Internal Med, Davis, CA 95616 USA

来源：

FEBS LETTERS | 2003年 / 544卷 / 1-3期

关键词：

prolactin; prolactin receptor; nitric oxide; iNOS; pro-inflammatory cytokine; STAT-5b; IRF-1;

D O I：

10.1016/S0014-5793(03)00499-X

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

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. (C) 2003 Published by Elsevier Science B.V. on behalf of the Federation of European Biochemical Societies.

引用

页码：171 / 175

页数：5

共 33 条

[31] Multiple Stat complexes interact at the interferon regulatory factor-1 interferon-gamma activation sequence in prolactin-stimulated Nb2 T cells [J].