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Mitochondrial extracellular signal‐regulated kinases 1/2 (ERK1/2) are modulated during brain development
Author(s) -
Alonso Mariana,
Melani Mariana,
Converso Daniela,
Jaitovich Ariel,
Paz Cristina,
Carreras M. Cecilia,
Medina Jorge H.,
Poderoso Juan J.
Publication year - 2004
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2004.02323.x
Subject(s) - microbiology and biotechnology , mitochondrion , kinase , mapk/erk pathway , biology , organelle , extracellular , intracellular , signal transduction , intermembrane space , biochemistry , bacterial outer membrane , escherichia coli , gene
Intracellular activation and trafficking of extracellular signal‐regulated protein kinases (ERK) play a significant role in cell cycle progression, contributing to developmental brain activities. Additionally, mitochondria participate in cell signalling through energy‐linked functions, redox metabolism and activation of pro‐ or anti‐apoptotic proteins. The purpose of the present study was to analyze the presence of ERK1/2 in mitochondria during rat brain development. Immunoblotting, immune electron microscopy and activity assays demonstrated that ERK1/2 are present in fully active brain mitochondria at the outer membrane/intermembrane space fraction. Besides, it was observed that ERK1/2 translocation to brain mitochondria follows a developmental pattern which is maximal between E19‐P2 stages and afterwards declines at P3, just before maximal translocation to nucleus, and up to adulthood. Most of mitochondrial ERK1/2 were active; upstream phospho‐MAPK/ERK kinases (MEK1/2) were also detected in the brain organelles. Mitochondrial phospho‐ERK1/2 increased at 1 μ m hydrogen peroxide (H 2 O 2 ) concentration, but it decreased at higher 50–100 μ m H 2 O 2 , almost disappearing after the organelles were maximally stimulated to produce H 2 O 2 with antimycin. Our results suggest that developmental mitochondrial activation of ERK1/2 cascade contributes to its nuclear translocation effects, providing information about mitochondrial energetic and redox status to the proliferating/differentiating nuclear pathways.