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Extracellular signal-regulated kinase 1/2 plays a pro-life role in experimental brain stem death via MAPK signal-interacting kinase at rostral ventrolateral medulla

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As the origin of a life-and-death signal detected from systemic arterial pressure, which sequentially increases (pro-life) and decreases (pro-death) to reflect progressive dysfunction of central cardiovascular regulation during the advancement towards brain stem death in critically ill patients, the rostral ventrolateral medulla (RVLM) is a suitable neural substrate for mechanistic delineation of this fatal phenomenon. The present study assessed the hypothesis that extracellular signal-regulated kinase 1/2 (ERK1/2), a member of the mitogen-activated protein kinases (MAPKs) that is important for cell survival and is activated specifically by. | Chan et al. Journal of Biomedical Science 2010 17 17 http www.jbiomedsci.eom content 17 1 17 tì.NSC The cost of publication in Journal of Biomedical Science Is borne by the National Science Council Taiwan JOURNAL OF BIOMEDICAL SCIENCE RESEARCH Open Access Extracellular signal-regulated kinase 1 2 plays a pro-life role in experimental brain stem death via MAPK signal-interacting kinase at rostral ventrolateral medulla Samuel HH Chan Enya YH Sun Alice YW Chang Abstract Background As the origin of a life-and-death signal detected from systemic arterial pressure which sequentially increases pro-life and decreases pro-death to reflect progressive dysfunction of central cardiovascular regulation during the advancement towards brain stem death in critically ill patients the rostral ventrolateral medulla RVLM is a suitable neural substrate for mechanistic delineation of this fatal phenomenon. The present study assessed the hypothesis that extracellular signal-regulated kinase 1 2 ERK1 2 a member of the mitogen-activated protein kinases MAPKs that is important for cell survival and is activated specifically by MAPK kinase 1 2 MEK1 2 plays a pro-life role in RVLM during brain stem death. We further delineated the participation of MAPK signal-interacting kinase MNK a novel substrate of ERK in this process. Methods An experimental model of brain stem death that employed microinjection of the organophosphate insecticide mevinphos Mev 10 nmol bilaterally into RVLM of Sprague-Dawley rats was used in conjunction with cardiovascular pharmacological and biochemical evaluations. Results Results from ELISA showed that whereas the total ERK1 2 was not affected augmented phosphorylation of ERK1 2 at Thr202 and Tyr204 in RVLM occurred preferentially during the pro-life phase of experimental brain stem death. Furthermore pretreatment by microinjection into the bilateral RVLM of a specific ERK2 inhibitor ERK activation inhibitor peptide II 1 nmol a specific MEK1 2 inhibitor U0126 5 pmol or