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Role of protein kinase C and mitochondrial permeability transition pore in the neuroprotective effect of ceramide in ischemia‐induced cell death
Author(s) -
Agudo-López Alba,
Miguel Begoña G.,
Fernández Inmaculada,
Martínez Ana M.
Publication year - 2011
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.11.015
Subject(s) - mitochondrial permeability transition pore , ceramide , mptp , protein kinase c , microbiology and biotechnology , chemistry , mitochondrion , ceramide synthase , viability assay , lipid signaling , protein kinase a , reactive oxygen species , programmed cell death , kinase , biochemistry , cell , biology , apoptosis , enzyme , endocrinology , dopaminergic , dopamine
In this study, we investigated the role of protein kinase C (PKC) and mitochondrial permeability transition pore (mPTP) on the effect of ceramide in an in vitro model of ischemia in SH‐SY5Y neuroblastoma cells. In ischemic cell viability studies, a dual effect of ceramide was observed, depending on ceramide concentration. PKC isoforms are involved in the protective effect of low concentrations of ceramide. During ischemia, ceramide treatment leads to an increase in the formation of reactive oxygen species (ROS), which induces a controlled opening of mPTP. This fact prevents mitochondrial Ca 2+ overload, which is clearly protective.