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Parp and Cell Death or Protection in Rat Primary Astroglial Cell Cultures Under LPS/IFNγ Induced Proinflammatory Conditions

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Abstract

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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Acknowledgements

A special acknowledge goes to our scientific guide Prof. Anna Maria Giuffrida-Stella, that spent her life for the science and introduced us in this exciting world. This work was realized with the financial support of “Ricerca Ateneo”, University of Catania, FIRB RBNE03PX83, PRIN prot. 2005054147.

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  1. Department of Chemical Sciences, Section of Biochemistry and Molecular Biology, Medical Faculty, University of Catania, Viale A. Doria 6, 95125, Catania, Italy

    V. Spina-Purrello, D. Patti, A. M. Giuffrida-Stella & V. G. Nicoletti

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  1. V. Spina-Purrello
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  2. D. Patti
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  3. A. M. Giuffrida-Stella
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  4. V. G. Nicoletti
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Correspondence to V. G. Nicoletti.

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Special issue article in honor of Dr. Anna Maria Giuffrida-Stella.

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Spina-Purrello, V., Patti, D., Giuffrida-Stella, A.M. et al. Parp and Cell Death or Protection in Rat Primary Astroglial Cell Cultures Under LPS/IFNγ Induced Proinflammatory Conditions. Neurochem Res 33, 2583–2592 (2008). https://doi.org/10.1007/s11064-008-9835-1

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