Premium
98 Gene expression of transcription factors in apoptotic cerebellar granule cells
Author(s) -
Condorelli D.F.,
Copani A.,
Calogero A.,
Dell'Albani P.,
Nicoletti F.,
Stella A.M. Giuffrida
Publication year - 1996
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/0736-5748(96)80289-9
Subject(s) - granule (geology) , microbiology and biotechnology , apoptosis , chemistry , gene expression , transcription (linguistics) , gene , biology , biochemistry , paleontology , linguistics , philosophy
Apoptotic death plays a major role in development, trauma qury responses, and age-associated deficits tn the nervous system where neurotrophins (NT) wn spare neurons from death under these condltlons. While theu mechanisms of actlon are diverse and overlappmg, NTs differentially enhance cellular defenses by stimulating antioxidant activity and pyridine nueleotide metabolism, critical to neuronal resistonce to md recuperation from injuq. While causal factors for neuronal death range from the inttinsic (best described for programmed cell death (PCD] in development) to the extrinsic [due to traumaand ischemia-mediated oxidatlve stress), we hypothesize that initially distinct regulatory pathways for death of NT-responsive neurons converge into common sipnalling pathways at the level of transcription factor activation. Our hypothesis IS that neuronal apoptosis due to oxidatlve stress results from dlsruption of glutathione (CSH) homeostasis and hanscription factors~gnalling that share elements with intrinsic neuronal death due to NT deprivation. We have found that NGF sparing from cell death involves the sctivatlon of the NF-KB and AP-I transcription factors. We found evidence for apoptosis and altered transcription factor signal transduction pathways in aged and oridatively stressed brain. Supported in part by NINDS NS18708, NS-33288, NS-3 1998 This is publication 46a from USPHS grant PO1 AG-10514 D.F. Condorellil, A. Copan?, A. Calogero’, P. Dell’Albti’, F. Nicolett? and A.M. Giuffrida Stella’ Institute of Biochemistry1 (School of Medicine) and Institute of P~~~o~o~~J (School of Pharmacy), University of Catania; Istituto di Neuroscienze, Neuromed’ (Potilli), Italy