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Article: Macrophage colony-stimulating factor reduces tert-butyl hydroperoxide induced oxidative injury to monocytes/macrophages

TitleMacrophage colony-stimulating factor reduces tert-butyl hydroperoxide induced oxidative injury to monocytes/macrophages
Authors
Issue Date1999
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosis
Citation
Atherosclerosis, 1999, v. 147 n. 1, p. 33-40 How to Cite?
AbstractThe transformation of macrophages into foam cells is an important event in the development of atherosclerosis, and the oxidative injury caused by oxidized low density lipoprotein (Ox-LDL) plays an essential role in that process. It has been proved that macrophage colony-stimulating factor (M-CSF) could prevent the progression of atherosclerosis in Watanabe heritable hypercholesterolemic (WHHL) rabbits. We proposed that the anti-atherogenic effect of M-CSF was partly associated with its protective effect on monocyte- derived macrophages from Ox-LDL induced oxidative injury. In order to prove this, we investigated the effect of M-CSF on the oxidative injury caused by tert-butyl hydroperoxide (tbOOH) to mouse peritoneal macrophages and U937/J774 cell lines. The results showed that M-CSF could protect mouse peritoneal macrophages from oxidative injury (presented by cell morphology and cell survival rate); L929 cell-conditioned medium (L929-CM) had the same effect as M-CSF; and anti-M-CSF monoclonal antibody could mostly block the protective effect of L929-CM on macrophages. L929-CM was proved to be also able to decrease the impact of plasma membrane fluidity in U937 and J774 cells treated with tbOOH. Incubation with tbOOH caused DNA fragmentation in U937 cells. The presence of L929-CM greatly reduced the number of apoptotic U937 cells characterized by DNA fragmentation. From these results, we concluded that M-CSF could protect monocytes/macrophages from oxidative injury. It may be one of the mechanisms which explain the anti-atherogenic effect of exogenous M-CSF in WHHL rabbits.
Persistent Identifierhttp://hdl.handle.net/10722/178654
ISSN
2015 Impact Factor: 3.942
2015 SCImago Journal Rankings: 1.819
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorPang, ZJen_US
dc.contributor.authorZhou, Men_US
dc.contributor.authorChen, Yen_US
dc.contributor.authorWan, Jen_US
dc.date.accessioned2012-12-19T09:48:58Z-
dc.date.available2012-12-19T09:48:58Z-
dc.date.issued1999en_US
dc.identifier.citationAtherosclerosis, 1999, v. 147 n. 1, p. 33-40en_US
dc.identifier.issn0021-9150en_US
dc.identifier.urihttp://hdl.handle.net/10722/178654-
dc.description.abstractThe transformation of macrophages into foam cells is an important event in the development of atherosclerosis, and the oxidative injury caused by oxidized low density lipoprotein (Ox-LDL) plays an essential role in that process. It has been proved that macrophage colony-stimulating factor (M-CSF) could prevent the progression of atherosclerosis in Watanabe heritable hypercholesterolemic (WHHL) rabbits. We proposed that the anti-atherogenic effect of M-CSF was partly associated with its protective effect on monocyte- derived macrophages from Ox-LDL induced oxidative injury. In order to prove this, we investigated the effect of M-CSF on the oxidative injury caused by tert-butyl hydroperoxide (tbOOH) to mouse peritoneal macrophages and U937/J774 cell lines. The results showed that M-CSF could protect mouse peritoneal macrophages from oxidative injury (presented by cell morphology and cell survival rate); L929 cell-conditioned medium (L929-CM) had the same effect as M-CSF; and anti-M-CSF monoclonal antibody could mostly block the protective effect of L929-CM on macrophages. L929-CM was proved to be also able to decrease the impact of plasma membrane fluidity in U937 and J774 cells treated with tbOOH. Incubation with tbOOH caused DNA fragmentation in U937 cells. The presence of L929-CM greatly reduced the number of apoptotic U937 cells characterized by DNA fragmentation. From these results, we concluded that M-CSF could protect monocytes/macrophages from oxidative injury. It may be one of the mechanisms which explain the anti-atherogenic effect of exogenous M-CSF in WHHL rabbits.en_US
dc.languageengen_US
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosisen_US
dc.relation.ispartofAtherosclerosisen_US
dc.subject.meshAnimalsen_US
dc.subject.meshArteriosclerosis - Metabolismen_US
dc.subject.meshCell Lineen_US
dc.subject.meshCell Survival - Drug Effectsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCulture Media, Conditioneden_US
dc.subject.meshDna Fragmentation - Drug Effectsen_US
dc.subject.meshLipoproteins, Ldl - Physiology - Toxicityen_US
dc.subject.meshMacrophage Colony-Stimulating Factor - Pharmacologyen_US
dc.subject.meshMacrophages, Peritoneal - Cytology - Drug Effects - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Fluidity - Drug Effectsen_US
dc.subject.meshMiceen_US
dc.subject.meshMonocytes - Drug Effects - Metabolismen_US
dc.subject.meshOxidation-Reductionen_US
dc.subject.meshOxidative Stress - Drug Effectsen_US
dc.subject.meshTert-Butylhydroperoxide - Toxicityen_US
dc.titleMacrophage colony-stimulating factor reduces tert-butyl hydroperoxide induced oxidative injury to monocytes/macrophagesen_US
dc.typeArticleen_US
dc.identifier.emailWan, J: jmfwan@hku.hken_US
dc.identifier.authorityWan, J=rp00798en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0021-9150(99)00159-8en_US
dc.identifier.pmid10525122-
dc.identifier.scopuseid_2-s2.0-0032853093en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032853093&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume147en_US
dc.identifier.issue1en_US
dc.identifier.spage33en_US
dc.identifier.epage40en_US
dc.identifier.isiWOS:000083519900005-
dc.publisher.placeIrelanden_US
dc.identifier.scopusauthoridPang, ZJ=7103343225en_US
dc.identifier.scopusauthoridZhou, M=7403506134en_US
dc.identifier.scopusauthoridChen, Y=16745998900en_US
dc.identifier.scopusauthoridWan, J=8930305000en_US

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