Abstract:
: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.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Corbacho AM,Macotela Y,Nava G,Eiserich JP,Cross CE,Martínez de la Escalera G,Clapp Cdoi
10.1016/s0014-5793(03)00499-xkeywords:
subject
Has Abstractpub_date
2003-06-05 00:00:00pages
171-5issue
1-3eissn
0014-5793issn
1873-3468pii
S001457930300499Xjournal_volume
544pub_type
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