We are analyzing https://link.springer.com/article/10.1007/s11064-008-9835-1.

Title:
Parp and Cell Death or Protection in Rat Primary Astroglial Cell Cultures Under LPS/IFNγ Induced Proinflammatory Conditions | Neurochemical Research
Description:
The enzyme poly(ADP-ribose)polymerase (PARP) has a leader role in the DNA damage survey mechanisms by its nick-sensor function, but it is also involved in the early events of the programmed cell death, particularly during inflammatory injury, as a coactivator of NF-kB. In the present study, we evaluated the PARP involvement in the mechanisms of protection and/or cell death in rat astroglial cell cultures during the early phase of proinflammatory commitment after lipopolysaccharide and interferon gamma treatment. According with the recent findings that PARP-1 phosphorylation by MAPK/ERK-2 pathway seems to modulate PARP activation, in time course experiments we demonstrated that a very early PARP activation and expression is able to trigger a cell death pathway, DNA damage independent, during strong proinflammatory insults, maintaining its role of guardian of the genome stability only during the normal cell cycling.
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Keywords {🔍}

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Topics {✒️}

γ-irradiated balb/3t3 fibroblasts month download article/chapter dna double-strand breaks glucocorticoid-mediated cell lysis parp-1 reduces alpha-synuclein ca2+/mg2+-dependent endonuclease extracellular signal-regulated kinases mek/erk pathway extracellular signal-regulated kinase nf-κb transcriptional activation defective nf-kappab activation mnng-treated hela cells growth-phase-dependent response parp-1-induced cell death polymerase-1-dependent cell death erk signaling pathway redox-dependent transcriptional regulation nitric oxide donors article spina-purrello dna strand breaks anna maria giuffrida-stella full article pdf de menissier murcia lps-stimulated j774 cell death pathway mapk/erk-2 pathway glutamate-induced neurotoxicity astroglial cell cultures related subjects privacy choices/manage cookies dna damage response pro-apoptotic factors necrotic death induced differential gene expression vivo oxidative stress glial inos expression necrotic cell death nf-kb activation adp-ribose polymerase-1 regulates programmed cell death strong proinflammatory insults dual-key mechanism inducing neuronal death conditions privacy policy parp-1 nhej pathway dna damage independent oxidative dna damage apoptotic neuronal death stalled replication forks parp1-dependent kinetics

Questions {❓}

Chiarugi A (2002) Poly(ADP-ribose) polymerase: killer or conspirator?
Nicoletti VG, Giuffrida-Stella AM (2003) Role of PARP under stress conditions: cell death or protection?
Shall S, De Murcia G (2000) Poly(ADP-ribose) polimerase-1: what we have learned from the deficient mouse model?

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