Contrasting actions of prolonged mitogen-activated protein kinase activation on cell survival

Bahareh Badrian, Tammy Casey, Chooi-May Lai, Elizabeth Rakoczy, Peter Arthur, M.A. Bogoyevitch

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)


Activation of the ERK mitogen-activated protein kinase pathway has been implicated in pro-survival and cellular protective mechanisms. so that chronic ERK activation may be a useful therapeutic strategy. Here, we further explored the consequences of prolonged ERK activation following expression of constitutively active form of MEK, MEK-EE, in cardiac myocytes. We confirmed that chronic MEK-EE overexpression halved myocyte death following glucose deprivation, but surprisingly this was not associated with preserved intracellular ATP levels. Whilst activities of a number of antioxidant enzymes were not altered upon MEK-EE expression, paradoxically Cu/Zn superoxide dismutase activity was almost halved upon MEK-EE expression. When we then exposed myocytes to the superoxide generator menadione, we observed significantly higher death of MEK-EE expressing myocytes. Pre-incubation with U0126 inhibited menadione-induced death. Our results are the first to show that MEK-ERK signalling can act to increase or decrease cell survival., the outcome depending on the form of stress stimulus encountered. (c) 2006 Elsevier Inc. All rights reserved.
Original languageEnglish
Pages (from-to)843-850
JournalBiochemical and Biophysical Research Communications
Issue number2
Publication statusPublished - 2006


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