Cell cycle induction in post-mitotic neurons proceeds in concert with the initial phase of programmed cell death in rat.
Neuronal programmed cell death (PCD) is increasingly becoming recognized as a dynamic process that may be amenable to resolution. Critical to this resolution is the identification of the cellular pathways that modulate the initial stages of apoptotic death. In this regard, we examined whether the activation of a latent cell cycle was associated with the initial phase of PCD. We demonstrate that free radical nitric oxide induced PCD results in the rapid generation of membrane phosphatidylserine residue exposure. This early phase of PCD functions in parallel with an untoward attempt to enter the cell cycle in the same population of post-mitotic neurons. We therefore offer an attractive molecular target to prevent or reverse neuronal PCD by elucidating a novel mechanism through which the majority of neurons meet their demise by attempting to enter a latent cell cycle.
Lin
S H
SH
Division of Cellular and Molecular Cerebral Ischemia, Wayne State University School of Medicine, Detroit, MI 48201, USA.
Chong
Z Z
ZZ
Maiese
K
K
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001973:Bromodeoxyuridine / Q000032:analysis; D002478:Cells, Cultured; D005609:Free Radicals / Q000378:metabolism; D006624:Hippocampus / Q000166:cytology; D020287:In Situ Nick-End Labeling; D008297:Male; D008938:Mitosis; D009474:Neurons / Q000737:chemistry / Q000166:cytology* / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D010718:Phosphatidylserines / Q000032:analysis; D018809:Proliferating Cell Nuclear Antigen / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley
D005609:Free Radicals; D010718:Phosphatidylserines; D018809:Proliferating Cell Nuclear Antigen; D009569:Nitric Oxide; D001973:Bromodeoxyuridine