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Cytokine induction of prolactin receptors mediates prolactin inhibition of nitric oxide synthesis in pulmonary fibroblasts
Author(s) -
Corbacho Ana M.,
Macotela Yazmin,
Nava Gabriel,
Eiserich Jason P.,
Cross Carroll E.,
Martı́nez de la Escalera Gonzalo,
Clapp Carmen
Publication year - 2003
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(03)00499-x
Subject(s) - prolactin , cytokine , stat protein , receptor , nitric oxide synthase , nitric oxide , mediator , medicine , endocrinology , microbiology and biotechnology , signal transduction , inflammation , biology , activator (genetics) , prolactin receptor , transcription factor , chemistry , stat3 , immunology , hormone , biochemistry , gene
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.