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Mediators of Interferon γ-Initiated Signaling in Bovine Luteal Cells
Ist Teil von
Biology of reproduction, 2001-05, Vol.64 (5), p.1481
Ort / Verlag
Society for the Study of Reproduction
Erscheinungsjahr
2001
Quelle
Free E-Journal (出版社公開部分のみ)
Beschreibungen/Notizen
Interferon gamma (IFNγ) has been implicated as a mediator of luteal steroidogenesis and cell fate. IFNγ-initiated signaling
events, although implied by studies in cell lines, have yet to be described in primary luteal cells. The objective of these
studies was to begin to characterize IFNγ-initiated signaling within luteal cells. Dispersed bovine luteal cell cultures were
challenged with increasing levels of bovine recombinant IFNγ (0â1000 U) or IFNγ (200 U) in the presence or absence of tumor
necrosis factor α (TNFα, 10 ng/ml) over time (short term, 0â60 min; long term, 0, 24, 48 h). Fractionated or total cell lysates
were evaluated by the Western blotting technique to determine the changes in the levels of signal transducers and activators
of transcription (STAT), interferon regulatory factor 1 (IRF-1), and I kappa B α (IκB-α). Utilizing antibodies that recognize
the nonphosphorylated forms of STAT-1 and STAT-3, it was determined that levels of STAT-1 and STAT-3 in total cell lysates
were constitutively expressed and did not change in response to treatment with IFNγ or TNFα. In contrast, nuclear levels of
STAT-1 and phosphorylated STAT-3 were elevated in a time-dependent manner in response to IFNγ treatment. Furthermore, IFNγ
and TNFα treatment elevated levels of IRF-1 within 2 h. TNFα-induced increases in the levels of IRF-1 were transient, whereas
the levels of IRF-1 in response to IFNγ treatment remained elevated at 48 h. These data suggest that IFNγ treatment can activate
members of the STAT pathway, resulting in increased levels of IRF-1. TNFα treatment induced a rapid decrease in the [bu791]levels
of IκB-α. IFNγ treatment did not alter the levels of IκB-α and failed to inhibit the TNFα-initiated decrease in the levels
of IκB-α. The present experiment demonstrates that the steroidogenic cells of the corpus luteum have the capacity to respond
to IFNγ via activation of STAT and IRF-1, providing further evidence that IFNγ may be involved in the luteolytic process.
These data also suggest that IFNγ does not signal through the nuclear factor κ B cell survival signaling pathway.
Sprache
Englisch
Identifikatoren
ISSN: 0006-3363
eISSN: 1529-7268
DOI: 10.1095/biolreprod64.5.1481
Titel-ID: cdi_highwire_smallpub3_www64_5_1481
Format
–
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