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

Current evidence suggests that stress-induced apoptosis is mediated through the activation of the mitogen-activated protein kinase (MAPK) signaling ca scade. We hypothesize that stress-related signaling events documented in ot her cell lines may also occur in the corpus luteum. To test this, cultured bovine luteal cells were exposed to UV irradiation and harvested at differe nt intervals (0, 30, 120, 240 and 360 min) for analysis of protein or apopt otic cell death. In response to UV treatment cellular levels of phosphoryla ted 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 t hose observed in response to tumor necrosis factor cc, a cytokine implicate d 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 even ts in the corpus luteum are similar to those observed in unrelated cell typ es. Thus, stress-related signaling events may play a role in luteal regress ion. (C) 2000 Published by Elsevier Science Ireland Ltd. All rights reserve d.