title: The preconditioning modified neuronal expression of apoptosis-related proteins of Bcl-2 superfamily following severe hypobaric hypoxia in rats.
abstract: The patterns of expression of the Bcl-2, Bax, and Bcl-xL proteins were examined immunocytochemically in rat hippocampus and neocortex after severe hypobaric hypoxia (180 Torr for 3 h) and severe hypoxia preconditioned by intermittent mild hypoxia (360 Torr for 2 h daily, for 3 consecutive days, 24 h prior to severe hypoxia). As revealed by TUNEL assay, severe hypobaric hypoxia produced extensive apoptotic damage to the neurons of hippocampal CA1-CA4 and the neocortex but not the dentate gyrus granule cells. Remarkable posthypoxic up-regulation of Bax expression maximal at 24 h was detected in the CA1-CA4 areas of hippocampus and neocortex 3-72 h after severe hypoxia. The preconditioning to severe hypoxia protected neurons from the posthypoxic apoptotic transformations, the up-regulation of Bax expression, and resulted in persistent overexpression of Bcl-2 and Bcl-xL. We conclude that the protective action of hypoxic preconditioning is at least in part mediated by shifting of neuronal Bax/Bcl-2-Bcl-xL ratio to a favor of antiapoptotic proteins Bcl-2 and Bcl-xL.
authors.affiliation: The Laboratory of Neuroendocrinology, Pavlov Institute of Physiology, Russian Academy of Sciences, Makarova emb. 6, St. Petersburg 199034, Russia.
authors.forename: Elena
authors.initials: E
authors.lastname: Rybnikova
authors.forename: Nadezhda
authors.initials: N
authors.lastname: Sitnik
authors.forename: Tatjana
authors.initials: T
authors.lastname: Gluschenko
authors.forename: Ekaterina
authors.initials: E
authors.lastname: Tjulkova
authors.forename: Michail O
authors.initials: MO
authors.lastname: Samoilov
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001274:Atmospheric Pressure; D002544:Cerebral Infarction / Q000378:metabolism* / Q000503:physiopathology; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D002534:Hypoxia, Brain / Q000378:metabolism* / Q000503:physiopathology; D007150:Immunohistochemistry; D019194:Ischemic Preconditioning / Q000379:methods*; D008297:Male; D051336:Mitochondrial Membranes / Q000378:metabolism; D019579:Neocortex / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D009410:Nerve Degeneration / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction / Q000502:physiology; D013997:Time Factors; D051028:bcl-2-Associated X Protein / Q000378:metabolism; D051020:bcl-X Protein / Q000378:metabolism
chemical_list: C494813:Bcl2l1 protein, rat; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D051020:bcl-X Protein