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

Ana M. Corbacho, Yazmin Macotela, Gabriel Nava, Jason P. Eiserich, Carroll E Cross, Gonzalo Martínez De La Escalera, Carmen Clapp

Research output: Contribution to journalArticlepeer-review

31 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)171-175
Number of pages5
JournalFEBS Letters
Volume544
Issue number1-3
DOIs
StatePublished - Jun 5 2003

Keywords

  • iNOS
  • IRF-1
  • Nitric oxide
  • Pro-inflammatory cytokine
  • Prolactin
  • Prolactin receptor
  • STAT-5b

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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