Mediators of interferon γ-initiated signaling in bovine luteal cells

J. Suter, I. R. Hendry, L. Ndjountche, K. Obholz, J. K. Pru, J. S. Davis, B. R. Rueda

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

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 (0-1000 U) or IFNγ (200 U) in the presence or absence of tumor necrosis factor α (TNFα, 10 ng/ml) over time (short term, 0-60 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 non-phosphorylated 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 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.

Original languageEnglish (US)
Pages (from-to)1481-1486
Number of pages6
JournalBiology of reproduction
Volume64
Issue number5
DOIs
StatePublished - Jan 1 2001

Fingerprint

Luteal Cells
Interferons
Interferon-gamma
Interferon Regulatory Factor-1
I-kappa B Proteins
STAT1 Transcription Factor
STAT3 Transcription Factor
Transducers
Corpus Luteum

Keywords

  • Corpus luteum
  • Corpus luteum function
  • Cytokines
  • Signal transduction

ASJC Scopus subject areas

  • Cell Biology

Cite this

Suter, J., Hendry, I. R., Ndjountche, L., Obholz, K., Pru, J. K., Davis, J. S., & Rueda, B. R. (2001). Mediators of interferon γ-initiated signaling in bovine luteal cells. Biology of reproduction, 64(5), 1481-1486. https://doi.org/10.1095/biolreprod64.5.1481

Mediators of interferon γ-initiated signaling in bovine luteal cells. / Suter, J.; Hendry, I. R.; Ndjountche, L.; Obholz, K.; Pru, J. K.; Davis, J. S.; Rueda, B. R.

In: Biology of reproduction, Vol. 64, No. 5, 01.01.2001, p. 1481-1486.

Research output: Contribution to journalArticle

Suter, J, Hendry, IR, Ndjountche, L, Obholz, K, Pru, JK, Davis, JS & Rueda, BR 2001, 'Mediators of interferon γ-initiated signaling in bovine luteal cells', Biology of reproduction, vol. 64, no. 5, pp. 1481-1486. https://doi.org/10.1095/biolreprod64.5.1481
Suter, J. ; Hendry, I. R. ; Ndjountche, L. ; Obholz, K. ; Pru, J. K. ; Davis, J. S. ; Rueda, B. R. / Mediators of interferon γ-initiated signaling in bovine luteal cells. In: Biology of reproduction. 2001 ; Vol. 64, No. 5. pp. 1481-1486.
@article{94681b192bc54c3c92f42147ee4dd3ac,
title = "Mediators of interferon γ-initiated signaling in bovine luteal cells",
abstract = "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 (0-1000 U) or IFNγ (200 U) in the presence or absence of tumor necrosis factor α (TNFα, 10 ng/ml) over time (short term, 0-60 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 non-phosphorylated 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 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.",
keywords = "Corpus luteum, Corpus luteum function, Cytokines, Signal transduction",
author = "J. Suter and Hendry, {I. R.} and L. Ndjountche and K. Obholz and Pru, {J. K.} and Davis, {J. S.} and Rueda, {B. R.}",
year = "2001",
month = "1",
day = "1",
doi = "10.1095/biolreprod64.5.1481",
language = "English (US)",
volume = "64",
pages = "1481--1486",
journal = "Biology of Reproduction",
issn = "0006-3363",
publisher = "Society for the Study of Reproduction",
number = "5",

}

TY - JOUR

T1 - Mediators of interferon γ-initiated signaling in bovine luteal cells

AU - Suter, J.

AU - Hendry, I. R.

AU - Ndjountche, L.

AU - Obholz, K.

AU - Pru, J. K.

AU - Davis, J. S.

AU - Rueda, B. R.

PY - 2001/1/1

Y1 - 2001/1/1

N2 - 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 (0-1000 U) or IFNγ (200 U) in the presence or absence of tumor necrosis factor α (TNFα, 10 ng/ml) over time (short term, 0-60 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 non-phosphorylated 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 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.

AB - 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 (0-1000 U) or IFNγ (200 U) in the presence or absence of tumor necrosis factor α (TNFα, 10 ng/ml) over time (short term, 0-60 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 non-phosphorylated 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 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.

KW - Corpus luteum

KW - Corpus luteum function

KW - Cytokines

KW - Signal transduction

UR - http://www.scopus.com/inward/record.url?scp=0035040010&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035040010&partnerID=8YFLogxK

U2 - 10.1095/biolreprod64.5.1481

DO - 10.1095/biolreprod64.5.1481

M3 - Article

C2 - 11319155

AN - SCOPUS:0035040010

VL - 64

SP - 1481

EP - 1486

JO - Biology of Reproduction

JF - Biology of Reproduction

SN - 0006-3363

IS - 5

ER -