https://scholars.lib.ntu.edu.tw/handle/123456789/569289
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.author | Chang M.-C. | en_US |
dc.contributor.author | LI-DEH LIN | en_US |
dc.contributor.author | Chuang F.-H. | en_US |
dc.contributor.author | Chan C.-P. | en_US |
dc.contributor.author | TONG-MEI WANG | en_US |
dc.contributor.author | JANG-JAER LEE | en_US |
dc.contributor.author | Jeng P.-Y. | en_US |
dc.contributor.author | WAN-YU TSENG | en_US |
dc.contributor.author | Lin H.-J. | en_US |
dc.contributor.author | JIIANG-HUEI JENG | en_US |
dc.date.accessioned | 2021-07-05T06:23:14Z | - |
dc.date.available | 2021-07-05T06:23:14Z | - |
dc.date.issued | 2012 | - |
dc.identifier.issn | 1742-7061 | - |
dc.identifier.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-84856555643&doi=10.1016%2fj.actbio.2011.09.011&partnerID=40&md5=33dd5c9cb29087d63e40d5be2d4f8937 | - |
dc.identifier.uri | https://scholars.lib.ntu.edu.tw/handle/123456789/569289 | - |
dc.description.abstract | Biocompatibility of dentin bonding agents (DBA) and composite resin may affect the treatment outcome (e.g., healthy pulp, pulpal inflammation, pulp necrosis) after operative restoration. Bisphenol-glycidyl methacrylate (BisGMA) is one of the major monomers present in DBA and resin. Prior studies focused on salivary esterase for metabolism and degradation of resin monomers clinically. This study found that human dental pulp cells expressed mainly carboxylesterase-2 (CES2) and smaller amounts of CES1A1 and CES3 isoforms. Exposure to BisGMA stimulated CES isoforms expression of pulp cells, and this event was inhibited by catalase. Exogenous addition of porcine esterase prevented BisGMA- and DBA-induced cytotoxicity. Interestingly, inhibition of CES by bis(p-nitrophenyl) phosphate (BNPP) and CES2 by loperamide enhanced the cytotoxicity of BisGMA and DBA. Addition of porcine esterase or N-acetyl-l-cysteine prevented BisGMA-induced prostaglandin E2 (PGE2) and PGF2α production. In contrast, addition of BNPP and loperamide, but not mevastatin, enhanced BisGMA-induced PGE 2 and PGF2α production in dental pulp cells. These results suggest that BisGMA may induce the cytotoxicity and prostanoid production of pulp cells, leading to pulpal inflammation or necrosis via reactive oxygen species production. Expression of CES, especially CES2, in dental pulp cells can be an adaptive response to protect dental pulp against BisGMA-induced cytotoxicity and prostanoid release. Resin monomers are the main toxic components in DBA, and the ester group is crucial for monomer toxicity. ? 2011 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved. | - |
dc.relation.ispartof | Acta Biomaterialia | - |
dc.subject.classification | [SDGs]SDG3 | - |
dc.subject.other | Acrylic monomers; Amino acids; Biocompatibility; Cells; Dental composites; Enzymes; Esters; Pathology; Resins; Bisphenol-glycidyl methacrylate; Bisphenols; Carboxylesterases; Dental adhesives; Dental pulp; Dental pulp cells; Dentin bonding agents; Glycidyl methacrylate; Prostanoids; Resin monomer; Cytotoxicity; bis(4 nitrophenyl) phosphate; bisphenol glycidyl methacrylate; carboxylesterase; catalase; compactin; loperamide; monomer; prostaglandin E2; prostaglandin F2 alpha; prostanoid; reactive oxygen metabolite; unclassified drug; article; controlled study; cytotoxicity; hormone synthesis; human; human cell; priority journal; protein expression; tooth pulp; Sus | - |
dc.title | Carboxylesterase expression in human dental pulp cells: Role in regulation of BisGMA-induced prostanoid production and cytotoxicity | en_US |
dc.type | journal article | en |
dc.identifier.doi | 10.1016/j.actbio.2011.09.011 | - |
dc.identifier.pmid | 21951919 | - |
dc.identifier.scopus | 2-s2.0-84856555643 | - |
dc.relation.pages | 1380-1387 | - |
dc.relation.journalvolume | 8 | - |
dc.relation.journalissue | 3 | - |
item.openairetype | journal article | - |
item.fulltext | no fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.grantfulltext | none | - |
item.cerifentitytype | Publications | - |
crisitem.author.dept | Dentistry | - |
crisitem.author.dept | School of Dentistry | - |
crisitem.author.dept | Dentistry-NTUH | - |
crisitem.author.dept | Dentistry | - |
crisitem.author.dept | School of Dentistry | - |
crisitem.author.dept | Dentistry-NTUH | - |
crisitem.author.dept | Dentistry | - |
crisitem.author.dept | Dentistry-NTUH | - |
crisitem.author.dept | School of Dentistry | - |
crisitem.author.dept | Dentistry | - |
crisitem.author.dept | School of Dentistry | - |
crisitem.author.dept | Dentistry-NTUH | - |
crisitem.author.dept | Clinical Dentistry | - |
crisitem.author.dept | Dentistry-NTUH | - |
crisitem.author.dept | School of Dentistry | - |
crisitem.author.orcid | 0000-0002-6050-7394 | - |
crisitem.author.orcid | 0000-0002-9885-6899 | - |
crisitem.author.orcid | 0000-0003-0964-0840 | - |
crisitem.author.orcid | 0000-0002-9012-3703 | - |
crisitem.author.orcid | 0000-0002-2068-5380 | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
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