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Article: Activation of mitogen-activated protein kinases cellular signal transduction pathway in mammalian cells induced by silicon carbide nanowires

TitleActivation of mitogen-activated protein kinases cellular signal transduction pathway in mammalian cells induced by silicon carbide nanowires
Authors
KeywordsApoptosis
Cyclooxygenase-2
Genomic instability
Mitogen-activated protein kinases
Phosphorylation
Silicon carbide nanowires
Issue Date2010
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/biomaterials
Citation
Biomaterials, 2010, v. 31 n. 31, p. 7856-7862 How to Cite?
AbstractBecause of emerging biomedical applications of nanoscale materials, the behavior of cells in contact with nanoscale materials must be better understood. SiC nanostructures constitute a new class of biomaterials and have potential in many applications. In this study, the cellular signal transduction processes and toxicity mechanisms of silicon carbide nanowires (SiCNWs) are investigated. The Chinese hamster ovary (CHO) cells in contact with SiCNWs have significantly lower reproduction rates and genomic instability which may be the upstream event of cell apoptosis. Expression of the phosphorylated form of the mitogen-activated protein kinases (MAPKs) family including phosphorylated signal-regulated kinases (p-ERKs), phosphorylated c-Jun NH2-terminal kinases (p-JNKs), and phosphorylated p38-mitogen-activated protein kinases (p-p38) are observed at different time points during exposure to SiCNWs. Moreover, activation of the MAPKs family by phosphorylation which is an upstream event giving rise to expression of cyclooxygenase-2 (COX-2) is also observed. The specific inhibitors of the MAPKs family are found to restrain COX-2 high expression at some time points. Our results show that activation of the MAPKs cellular signaling pathway and over-expression of COX-2 are the main toxicity mechanisms in SiCNWs irritation. © 2010 Elsevier Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/139544
ISSN
2015 Impact Factor: 8.387
2015 SCImago Journal Rankings: 3.565
ISI Accession Number ID
Funding AgencyGrant Number
Chinese Academy of Sciences
City University of Hong Kong7008009
National High Technology Research and Development Program of China2009AA02Z416
National Natural Science Foundation of China
Funding Information:

The work was supported by the Knowledge Innovation Program of the Chinese Academy of Sciences, City University of Hong Kong Strategic Research Grant (SRG) No. 7008009. National High Technology Research and Development Program of China No. 2009AA02Z416, and National Natural Science Foundation of China No. 50902104.

References

 

DC FieldValueLanguage
dc.contributor.authorJiang, Jen_HK
dc.contributor.authorWang, Jen_HK
dc.contributor.authorZhang, Xen_HK
dc.contributor.authorHuo, Ken_HK
dc.contributor.authorWong, HMen_HK
dc.contributor.authorYeung, KWKen_HK
dc.contributor.authorZhang, Wen_HK
dc.contributor.authorHu, Ten_HK
dc.contributor.authorChu, PKen_HK
dc.date.accessioned2011-09-23T05:51:30Z-
dc.date.available2011-09-23T05:51:30Z-
dc.date.issued2010en_HK
dc.identifier.citationBiomaterials, 2010, v. 31 n. 31, p. 7856-7862en_HK
dc.identifier.issn0142-9612en_HK
dc.identifier.urihttp://hdl.handle.net/10722/139544-
dc.description.abstractBecause of emerging biomedical applications of nanoscale materials, the behavior of cells in contact with nanoscale materials must be better understood. SiC nanostructures constitute a new class of biomaterials and have potential in many applications. In this study, the cellular signal transduction processes and toxicity mechanisms of silicon carbide nanowires (SiCNWs) are investigated. The Chinese hamster ovary (CHO) cells in contact with SiCNWs have significantly lower reproduction rates and genomic instability which may be the upstream event of cell apoptosis. Expression of the phosphorylated form of the mitogen-activated protein kinases (MAPKs) family including phosphorylated signal-regulated kinases (p-ERKs), phosphorylated c-Jun NH2-terminal kinases (p-JNKs), and phosphorylated p38-mitogen-activated protein kinases (p-p38) are observed at different time points during exposure to SiCNWs. Moreover, activation of the MAPKs family by phosphorylation which is an upstream event giving rise to expression of cyclooxygenase-2 (COX-2) is also observed. The specific inhibitors of the MAPKs family are found to restrain COX-2 high expression at some time points. Our results show that activation of the MAPKs cellular signaling pathway and over-expression of COX-2 are the main toxicity mechanisms in SiCNWs irritation. © 2010 Elsevier Ltd.en_HK
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/biomaterialsen_HK
dc.relation.ispartofBiomaterialsen_HK
dc.subjectApoptosisen_HK
dc.subjectCyclooxygenase-2en_HK
dc.subjectGenomic instabilityen_HK
dc.subjectMitogen-activated protein kinasesen_HK
dc.subjectPhosphorylationen_HK
dc.subjectSilicon carbide nanowiresen_HK
dc.subject.meshCarbon Compounds, Inorganic - pharmacology-
dc.subject.meshMAP Kinase Signaling System - drug effects-
dc.subject.meshMitogen-Activated Protein Kinases - metabolism-
dc.subject.meshNanowires - chemistry - ultrastructure-
dc.subject.meshSilicon Compounds - pharmacology-
dc.titleActivation of mitogen-activated protein kinases cellular signal transduction pathway in mammalian cells induced by silicon carbide nanowiresen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0142-9612&volume=31&issue=31&spage=7856&epage=7862&date=2010&atitle=Activation+of+mitogen-activated+protein+kinases+cellular+signal+transduction+pathway+in+mammalian+cells+induced+by+silicon+carbide+nanowires-
dc.identifier.emailYeung, KWK:wkkyeung@hkucc.hku.hken_HK
dc.identifier.authorityYeung, KWK=rp00309en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.biomaterials.2010.07.024en_HK
dc.identifier.pmid20674003en_HK
dc.identifier.scopuseid_2-s2.0-77956010368en_HK
dc.identifier.hkuros192176en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77956010368&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume31en_HK
dc.identifier.issue31en_HK
dc.identifier.spage7856en_HK
dc.identifier.epage7862en_HK
dc.identifier.isiWOS:000282109100002-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridJiang, J=7401861084en_HK
dc.identifier.scopusauthoridWang, J=36068781200en_HK
dc.identifier.scopusauthoridZhang, X=7410267571en_HK
dc.identifier.scopusauthoridHuo, K=7004127177en_HK
dc.identifier.scopusauthoridWong, HM=35977282000en_HK
dc.identifier.scopusauthoridYeung, KWK=13309584700en_HK
dc.identifier.scopusauthoridZhang, W=7409430504en_HK
dc.identifier.scopusauthoridHu, T=25948400300en_HK
dc.identifier.scopusauthoridChu, PK=36040705700en_HK

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