STAT1‐NFκB crosstalk triggered by interferon gamma regulates noradrenaline‐induced pineal hormonal production
STAT1
Crosstalk
DOI:
10.1111/jpi.12599
Publication Date:
2019-07-29T17:09:21Z
AUTHORS (7)
ABSTRACT
Abstract Melatonin production by pineal glands is modulated several immune signals. The nuclear translocation of factor kappa‐B (NFκB) homodimers, lacking transactivation domains, once induced lipopolysaccharide (LPS) or tumor necrosis (TNF), inhibits the expression Aanat gene and synthesis noradrenaline (NA)‐induced melatonin. Interferon gamma (IFN‐γ), on other hand, increases melatonin synthesis. Furthermore, this cytokine activates signal transducer as well activator transcription 1 (STAT1) pathway, which was never evaluated a modulator before. Reports demonstrated that IFN‐γ might also activate NFκB. present study role STAT1‐NFκB crosstalk triggered regarding regulation NA‐induced glands’ hormonal production. Moreover, treatment increased transcription, in addition to N‐acetylserotonin (NAS) These effects were associated with STAT1 translocation, confirmed co‐immunoprecipitation promoter. Pharmacological enhancement augmented NAS Additionally, RelA‐NFκB subunits. blockade pathway prevented function. data show NFκB controls through synergistic mechanism, disclosing new integrative mechanism activity control.
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