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Article: Alterations in population dynamics of arterial smooth muscle cells during atherogenesis. IV. Evidence for a polyclonal origin of hypercholesterolemic diet induced atherosclerotic lesions in young swine

TitleAlterations in population dynamics of arterial smooth muscle cells during atherogenesis. IV. Evidence for a polyclonal origin of hypercholesterolemic diet induced atherosclerotic lesions in young swine
Authors
Issue Date1976
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yexmp
Citation
Experimental And Molecular Pathology, 1976, v. 24 n. 2, p. 244-260 How to Cite?
AbstractThe purpose of this study was to determine whether atherosclerotic lesions developing in young swine fed hypercholesterolemic (HC) diets were monoclonal or polyclonal in origin. The approach involved labeling arterial cells with tritiated thymidine prior to feeding the HC diet. Baseline swine were sacrificed and radioautography studies carried out to determine baseline labeling indices and grain number distributions in media and in intimal cellular masses (cushions). Remaining swine were then fed an HC diet for 30-60 days before sacrificing and making the same type determinations as with the baseline swine on putative active lesions and media. If a lesion arose from a single cell (or multiple unlabeled cells) labeling indices would be expected to be greatly reduced without a change in grain number patterns. This was not observed in any of the 14 putative lesions that were studied. If the lesion arose from divisions by multiple cells including labeled cells one would expect the proportion of cells with a high number of grains to be decreased, those with low numbers to be increased (since with division half the isotope goes to each daughter cell) and this to be reflected in the grain count. This occurred in 9 of the putative lesions, indicating multicellular origin. In 5 there were neither change in grain number distributions nor reduction in labeling indices. Hence, these showed no division activity during the period of study; they were classified as inactive lesions or preexisting cushions and provide no pertinent information for this study. The final conclusion was that all active lesions observed were polyclonal in origin. Further information was obtained by mathematical analysis on number of divisions made by the originally labeled cells; and considerable heterogeneity was observed, with some not dividing at all and others with progeny going through as many as 4 divisions.
Persistent Identifierhttp://hdl.handle.net/10722/178399
ISSN
2015 Impact Factor: 2.638
2015 SCImago Journal Rankings: 1.130
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorThomas, WAen_US
dc.contributor.authorFlorentin, RAen_US
dc.contributor.authorReiner, JMen_US
dc.contributor.authorLee, WMen_US
dc.contributor.authorLee, KTen_US
dc.date.accessioned2012-12-19T09:47:29Z-
dc.date.available2012-12-19T09:47:29Z-
dc.date.issued1976en_US
dc.identifier.citationExperimental And Molecular Pathology, 1976, v. 24 n. 2, p. 244-260en_US
dc.identifier.issn0014-4800en_US
dc.identifier.urihttp://hdl.handle.net/10722/178399-
dc.description.abstractThe purpose of this study was to determine whether atherosclerotic lesions developing in young swine fed hypercholesterolemic (HC) diets were monoclonal or polyclonal in origin. The approach involved labeling arterial cells with tritiated thymidine prior to feeding the HC diet. Baseline swine were sacrificed and radioautography studies carried out to determine baseline labeling indices and grain number distributions in media and in intimal cellular masses (cushions). Remaining swine were then fed an HC diet for 30-60 days before sacrificing and making the same type determinations as with the baseline swine on putative active lesions and media. If a lesion arose from a single cell (or multiple unlabeled cells) labeling indices would be expected to be greatly reduced without a change in grain number patterns. This was not observed in any of the 14 putative lesions that were studied. If the lesion arose from divisions by multiple cells including labeled cells one would expect the proportion of cells with a high number of grains to be decreased, those with low numbers to be increased (since with division half the isotope goes to each daughter cell) and this to be reflected in the grain count. This occurred in 9 of the putative lesions, indicating multicellular origin. In 5 there were neither change in grain number distributions nor reduction in labeling indices. Hence, these showed no division activity during the period of study; they were classified as inactive lesions or preexisting cushions and provide no pertinent information for this study. The final conclusion was that all active lesions observed were polyclonal in origin. Further information was obtained by mathematical analysis on number of divisions made by the originally labeled cells; and considerable heterogeneity was observed, with some not dividing at all and others with progeny going through as many as 4 divisions.en_US
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yexmpen_US
dc.relation.ispartofExperimental and Molecular Pathologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshArteries - Metabolism - Pathologyen_US
dc.subject.meshArteriosclerosis - Metabolism - Pathologyen_US
dc.subject.meshCell Divisionen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCholesterol, Dietaryen_US
dc.subject.meshDna - Biosynthesisen_US
dc.subject.meshDiet, Atherogenicen_US
dc.subject.meshHypercholesterolemia - Metabolism - Pathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMathematicsen_US
dc.subject.meshMuscle, Smooth - Metabolism - Pathologyen_US
dc.subject.meshSwineen_US
dc.subject.meshThymidine - Metabolismen_US
dc.titleAlterations in population dynamics of arterial smooth muscle cells during atherogenesis. IV. Evidence for a polyclonal origin of hypercholesterolemic diet induced atherosclerotic lesions in young swineen_US
dc.typeArticleen_US
dc.identifier.emailLee, WM: hrszlwm@hku.hken_US
dc.identifier.authorityLee, WM=rp00728en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/0014-4800(76)90009-5en_US
dc.identifier.pmid1261656-
dc.identifier.scopuseid_2-s2.0-0017236757en_US
dc.identifier.volume24en_US
dc.identifier.issue2en_US
dc.identifier.spage244en_US
dc.identifier.epage260en_US
dc.identifier.isiWOS:A1976BM74500009-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridThomas, WA=35551799800en_US
dc.identifier.scopusauthoridFlorentin, RA=6701862749en_US
dc.identifier.scopusauthoridReiner, JM=7102726225en_US
dc.identifier.scopusauthoridLee, WM=24799156600en_US
dc.identifier.scopusauthoridLee, KT=8054054000en_US

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