作者: Lara Macchioni , Lanfranco Corazzi , Vincenza Nardicchi , Roberta Mannucci , Cataldo Arcuri
关键词: Mitochondrion 、 Cell damage 、 Cell biology 、 Fumarase 、 Bacterial outer membrane 、 DiOC6 、 Membrane potential 、 Neurodegeneration 、 Phospholipase A2 、 Biology
摘要: Activation of brain mitochondrial phospholipase(s) A2 (PLA2) might contribute to cell damage and be involved in neurodegeneration. Despite the potential importance phenomenon, number, identities, properties these enzymes are still unknown. Here, we demonstrate that isolated mitochondria from rat cortex, incubated absence respiratory substrates, release a Ca2+-dependent PLA2 having biochemical characteristic secreted (sPLA2) immunoreacting with antibody raised against recombinant type IIA sPLA2 (sPLA2-IIA). Under identical conditions, no fumarase extramitochondrial medium was observed. The decreases when presence substrates such as ADP, malate, pyruvate, which causes an increase transmembrane determined by cytofluorimetric analysis using DiOC6(3) probe. treatment uncoupler carbonyl cyanide 3-chlorophenylhydrazone slightly enhances release. specific activity after removal outer membrane indicates enzyme is associated mitoplasts. localization has been confirmed electron microscopy U-251 astrocytoma cells confocal laser same PC-12 cells, where structurally similar isoform V-sPLA2 mainly nuclear localization. In addition sPLA2, contain another phospholipase Ca2+-independent sensitive bromoenol lactone, membrane. We hypothesize that, under reduced rate, sPLA2-IIA damage.