http://www.cnr.it/ontology/cnr/individuo/prodotto/ID202798
Human gingival fibroblasts stress response to HEMA: A role for protein kinase C alpha (Articolo in rivista)
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- Human gingival fibroblasts stress response to HEMA: A role for protein kinase C alpha (Articolo in rivista) (literal)
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- 2013-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1002/jbm.a.34337 (literal)
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Cataldi A, Zara S, Rapino M, Patruno A, di Giacomo V. (2013)
Human gingival fibroblasts stress response to HEMA: A role for protein kinase C alpha
in Journal of biomedical materials research. Part A; WILEY-BLACKWELL, 111 RIVER ST, HOBOKEN 07030-5774, NJ (Stati Uniti d'America)
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- Cataldi A, Zara S, Rapino M, Patruno A, di Giacomo V. (literal)
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- http://onlinelibrary.wiley.com/doi/10.1002/jbm.a.34337/abstract;jsessionid=B663A5B849C9283E8292AD2291380170.d04t02 (literal)
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- Univ G DAnnunzio, Dipartimento Med & Sci Invecchiamento, Chieti, Italy
Univ G DAnnunzio, Fac Farm, Cattedra Anat Umana, Chieti, Italy
Univ G DAnnunzio, Dipartimento Sci Farmaco, Chieti, Italy
CNR, Ist Genet Mol, Unita Chieti, I-00185 Rome, Italy (literal)
- Titolo
- Human gingival fibroblasts stress response to HEMA: A role for protein kinase C alpha (literal)
- Abstract
- 2-Hydroxyethil methacrylate (HEMA), component of dentin-bonding systems, by diffusing into oral cavity induces a cytotoxic response. HEMA determines reactive oxygen species (ROS) production activating specific signaling pathways, including protein kinases C (PKC). In addition, since a regulation is exerted by various PKCs on nitric oxide synthase (NOS) activation, our aim was to investigate the role of PKCs and the possible interplay with ROS and NO signaling system in human gingival fibroblasts (HGF) response to HEMA. Cultured HGFs were exposed to 3 mM (a subtoxic concentration) HEMA for 0, 24, or 96 h. Each experimental point were processed for flow cytometry, fluorescence microscopy, western blotting, and in vitro NOS specific activity analyses. Three millimolar HEMA reduces HGF proliferation less than 50% and increases apoptosis percentage up to 18%. Both ROS production and PKC a expression and activation are also increased 96 h after HEMA exposure. The increased specific activity of iNOS, inflammatory enzyme, accompanied by Bax high expression in HGF response to 96 h HEMA, document the occurrence of an inflammatory and apoptotic response to such agent. Interestingly, a reduced percentage of apoptotic cells and a reduced ROS production are evidenced in the presence of bisindolylmaleide VIII, a PKC a pharmacologic inhibitor. All in all, these results suggest that PKC a can mediate the inflammatory response disclosed by gingival fibroblasts to HEMA released monomers. (c) 2012 Wiley Periodicals, Inc. J Biomed Mater Res Part A, 2013. (literal)
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