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PARP-14 Promotes Survival of Mammalian α but Not β Pancreatic Cells Following Cytokine Treatment

PARP-14 (poly-ADP Ribose Polymerase-14), a member of the PARP family, belongs to the group of Bal proteins (B Aggressive Lymphoma). PARP-14 has recently appeared to be involved in the transduction pathway mediated by JNKs (c Jun N terminal Kinases), among which JNK2 promotes cancer cell survival. Se...

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Autores principales: D'Angeli, Floriana, Scalia, Marina, Cirnigliaro, Matilde, Satriano, Cristina, Barresi, Vincenza, Musso, Nicolò, Trovato-Salinaro, Angela, Barbagallo, Davide, Ragusa, Marco, Di Pietro, Cinzia, Purrello, Michele, Spina-Purrello, Vittoria
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6509146/
https://www.ncbi.nlm.nih.gov/pubmed/31130919
http://dx.doi.org/10.3389/fendo.2019.00271
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author D'Angeli, Floriana
Scalia, Marina
Cirnigliaro, Matilde
Satriano, Cristina
Barresi, Vincenza
Musso, Nicolò
Trovato-Salinaro, Angela
Barbagallo, Davide
Ragusa, Marco
Di Pietro, Cinzia
Purrello, Michele
Spina-Purrello, Vittoria
author_facet D'Angeli, Floriana
Scalia, Marina
Cirnigliaro, Matilde
Satriano, Cristina
Barresi, Vincenza
Musso, Nicolò
Trovato-Salinaro, Angela
Barbagallo, Davide
Ragusa, Marco
Di Pietro, Cinzia
Purrello, Michele
Spina-Purrello, Vittoria
author_sort D'Angeli, Floriana
collection PubMed
description PARP-14 (poly-ADP Ribose Polymerase-14), a member of the PARP family, belongs to the group of Bal proteins (B Aggressive Lymphoma). PARP-14 has recently appeared to be involved in the transduction pathway mediated by JNKs (c Jun N terminal Kinases), among which JNK2 promotes cancer cell survival. Several pharmacological PARP inhibitors are currently used as antitumor agents, even though they have also proved to be effective in many inflammatory diseases. Cytokine release from immune system cells characterizes many autoimmune inflammatory disorders, including type I diabetes, in which the inflammatory state causes β cell loss. Nevertheless, growing evidence supports a concomitant implication of glucagon secreting α cells in type I diabetes progression. Here, we provide evidence on the activation of a survival pathway, mediated by PARP-14, in pancreatic α cells, following treatment of αTC1.6 glucagonoma and βTC1 insulinoma cell lines with a cytokine cocktail: interleukin 1 beta (IL-1β), interferon gamma (IFN-γ) and tumor necrosis factor alpha (TNF-α). Through qPCR, western blot and confocal analysis, we demonstrated higher expression levels of PARP-14 in αTC1.6 cells with respect to βTC1 cells under inflammatory stimuli. By cytofluorimetric and caspase-3 assays, we showed the higher resistance of α cells compared to β cells to apoptosis induced by cytokines. Furthermore, the ability of PJ-34 to modulate the expression of the proteins involved in the survival pathway suggests a protective role of PARP-14. These data shed light on a poorly characterized function of PARP-14 in αTC1.6 cells in inflammatory contexts, widening the potential pharmacological applications of PARP inhibitors.
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spelling pubmed-65091462019-05-24 PARP-14 Promotes Survival of Mammalian α but Not β Pancreatic Cells Following Cytokine Treatment D'Angeli, Floriana Scalia, Marina Cirnigliaro, Matilde Satriano, Cristina Barresi, Vincenza Musso, Nicolò Trovato-Salinaro, Angela Barbagallo, Davide Ragusa, Marco Di Pietro, Cinzia Purrello, Michele Spina-Purrello, Vittoria Front Endocrinol (Lausanne) Endocrinology PARP-14 (poly-ADP Ribose Polymerase-14), a member of the PARP family, belongs to the group of Bal proteins (B Aggressive Lymphoma). PARP-14 has recently appeared to be involved in the transduction pathway mediated by JNKs (c Jun N terminal Kinases), among which JNK2 promotes cancer cell survival. Several pharmacological PARP inhibitors are currently used as antitumor agents, even though they have also proved to be effective in many inflammatory diseases. Cytokine release from immune system cells characterizes many autoimmune inflammatory disorders, including type I diabetes, in which the inflammatory state causes β cell loss. Nevertheless, growing evidence supports a concomitant implication of glucagon secreting α cells in type I diabetes progression. Here, we provide evidence on the activation of a survival pathway, mediated by PARP-14, in pancreatic α cells, following treatment of αTC1.6 glucagonoma and βTC1 insulinoma cell lines with a cytokine cocktail: interleukin 1 beta (IL-1β), interferon gamma (IFN-γ) and tumor necrosis factor alpha (TNF-α). Through qPCR, western blot and confocal analysis, we demonstrated higher expression levels of PARP-14 in αTC1.6 cells with respect to βTC1 cells under inflammatory stimuli. By cytofluorimetric and caspase-3 assays, we showed the higher resistance of α cells compared to β cells to apoptosis induced by cytokines. Furthermore, the ability of PJ-34 to modulate the expression of the proteins involved in the survival pathway suggests a protective role of PARP-14. These data shed light on a poorly characterized function of PARP-14 in αTC1.6 cells in inflammatory contexts, widening the potential pharmacological applications of PARP inhibitors. Frontiers Media S.A. 2019-05-03 /pmc/articles/PMC6509146/ /pubmed/31130919 http://dx.doi.org/10.3389/fendo.2019.00271 Text en Copyright © 2019 D'Angeli, Scalia, Cirnigliaro, Satriano, Barresi, Musso, Trovato-Salinaro, Barbagallo, Ragusa, Di Pietro, Purrello and Spina-Purrello. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Endocrinology
D'Angeli, Floriana
Scalia, Marina
Cirnigliaro, Matilde
Satriano, Cristina
Barresi, Vincenza
Musso, Nicolò
Trovato-Salinaro, Angela
Barbagallo, Davide
Ragusa, Marco
Di Pietro, Cinzia
Purrello, Michele
Spina-Purrello, Vittoria
PARP-14 Promotes Survival of Mammalian α but Not β Pancreatic Cells Following Cytokine Treatment
title PARP-14 Promotes Survival of Mammalian α but Not β Pancreatic Cells Following Cytokine Treatment
title_full PARP-14 Promotes Survival of Mammalian α but Not β Pancreatic Cells Following Cytokine Treatment
title_fullStr PARP-14 Promotes Survival of Mammalian α but Not β Pancreatic Cells Following Cytokine Treatment
title_full_unstemmed PARP-14 Promotes Survival of Mammalian α but Not β Pancreatic Cells Following Cytokine Treatment
title_short PARP-14 Promotes Survival of Mammalian α but Not β Pancreatic Cells Following Cytokine Treatment
title_sort parp-14 promotes survival of mammalian α but not β pancreatic cells following cytokine treatment
topic Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6509146/
https://www.ncbi.nlm.nih.gov/pubmed/31130919
http://dx.doi.org/10.3389/fendo.2019.00271
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