Stress-induced mitogen-activated protein kinase signaling in the corpus luteum

Bo R. Rueda, Isabel R. Hendry, Liliane Ndjountche, John Suter, John S. Davis

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


Current evidence suggests that stress-induced apoptosis is mediated through the activation of the mitogen-activated protein kinase (MAPK) signaling cascade. We hypothesize that stress-related signaling events documented in other cell lines may also occur in the corpus luteum. To test this, cultured bovine luteal cells were exposed to UV irradiation and harvested at different intervals (0, 30, 120, 240 and 360 min) for analysis of protein or apoptotic cell death. In response to UV treatment cellular levels of phosphorylated p38(MAPK) and jun-n-terminal kinase (JNK) were increased within 30 min and remained elevated over controls for the duration of the experiment. In contrast, the levels of the phosphorylated forms of p42(MAPK) and p44(MAPK) were dramatically reduced. The changes in MAPK signaling were similar to those observed in response to tumor necrosis factor α, a cytokine implicated in luteal regression. The UV-induced changes in MAPK phosphorylation were associated with an increase in caspase 3 activity and apoptotic cell death. Taken together, these data demonstrate that stress- induced signaling events in the corpus luteum are similar to those observed in unrelated cell types. Thus, stress-related signaling events may play a role in luteal regression. (C) 2000 Published by Elsevier Science Ireland Ltd.

Original languageEnglish (US)
Pages (from-to)59-67
Number of pages9
JournalMolecular and Cellular Endocrinology
Issue number1-2
StatePublished - Jun 20 2000
Externally publishedYes


  • Apoptosis
  • Cell signaling
  • Corpus luteum
  • MAP kinase

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Endocrinology


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