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Maternal Diet Supplemented with Methyl-Donors Protects against Atherosclerosis in F1 ApoE<sup>-/-</sup> Mice

dc.contributor.authorDelaney, C
dc.contributor.authorGarg, SK
dc.contributor.authorFernandes, C
dc.contributor.authorHoeltzel, M
dc.contributor.authorAllen, RH
dc.contributor.authorStabler, S
dc.contributor.authorYung, R
dc.contributor.editorStover, Cordula M
dc.coverage.spatialUnited States
dc.date.accessioned2024-05-06T19:31:48Z
dc.date.available2024-05-06T19:31:48Z
dc.date.issued2013-02-21
dc.identifier.issn1932-6203
dc.identifier.issn1932-6203
dc.identifier.urihttps://www.ncbi.nlm.nih.gov/pubmed/23437105
dc.identifier.urihttps://hdl.handle.net/2027.42/193099en
dc.description.abstractAtherosclerosis is an inflammatory condition of the arterial wall mediated by cells of both innate and adaptive immunity. T lymphocytes play an important role in orchestrating the pathogenic immune response involved in the acceleration of atherosclerosis. Previously, we have shown that a prenatal methyl-donor supplementation diet (MS), when fed to dams during pregnancy and lactation, decreased the T cell-mediated pro-inflammatory cytokine and chemokine response in F1 mice. In the current study, we report feeding Apolipoprotein E (ApoE-/-) deficient dams with the MS diet during pregnancy reduces atherosclerotic plaques in F1 mice that were fed high fat diet (HFD) after weaning. F1 mice from dams on the MS diet exhibited increased global T cell DNA methylation. T-cell chemokines and their receptors (in particular CCR2, CCR5, and CXCR3) play important roles in the inflammatory cell recruitment to vascular lesions. MS diet significantly reduced Ccr2 mRNA and protein expression in CD3+ T cells but not in CD11b+ monocytes in MS F1 mice relative to controls. F1 litter size, HFD consumption, body weight, and body fat were similar between control and MS diet groups. Moreover, serum thiol metabolite levels were similar between the two groups. However, MS diet is associated with significantly higher serum HDL and lower LDL+VLDL levels in comparison to F1 mice from dams on the control diet. Inflammatory cytokines (IL-17, TNF-α, IL-6) were also lower in MS F1 mice serum and conditioned media from T-cell culture. Altogether, these data suggest that the MS diet ameliorates development of atherosclerosis by inhibiting the T-cell Ccr2 expression, reducing inflammatory cytokines production and increasing serum HDL:LDL ratio. © 2013 Delaney et al.
dc.format.mediumPrint-Electronic
dc.languageeng
dc.publisherPublic Library of Science (PLoS)
dc.rightsLicence for published version: Creative Commons Attribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectAnimals
dc.subjectAorta
dc.subjectApolipoproteins E
dc.subjectAtherosclerosis
dc.subjectBody Composition
dc.subjectCholesterol
dc.subjectCrosses, Genetic
dc.subjectDiet
dc.subjectDiet, High-Fat
dc.subjectDietary Supplements
dc.subjectFeeding Behavior
dc.subjectFemale
dc.subjectGene Expression Regulation
dc.subjectInflammation Mediators
dc.subjectLipoproteins
dc.subjectLitter Size
dc.subjectLiver
dc.subjectLymphocyte Activation
dc.subjectMale
dc.subjectMethylation
dc.subjectMice
dc.subjectMonocytes
dc.subjectReceptors, CCR2
dc.subjectSulfhydryl Compounds
dc.subjectT-Lymphocytes
dc.subjectWeight Gain
dc.titleMaternal Diet Supplemented with Methyl-Donors Protects against Atherosclerosis in F1 ApoE<sup>-/-</sup> Mice
dc.typeArticle
dc.identifier.pmid23437105
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/193099/2/pone.0056253.pdf
dc.identifier.doi10.1371/journal.pone.0056253
dc.identifier.doihttps://dx.doi.org/10.7302/22744
dc.identifier.sourcePLoS ONE
dc.description.versionPublished version
dc.date.updated2024-05-06T19:31:45Z
dc.identifier.orcid0000-0002-8181-027X
dc.identifier.volume8
dc.identifier.issue2
dc.identifier.startpagee56253
dc.identifier.name-orcidDelaney, C
dc.identifier.name-orcidGarg, SK
dc.identifier.name-orcidFernandes, C
dc.identifier.name-orcidHoeltzel, M
dc.identifier.name-orcidAllen, RH
dc.identifier.name-orcidStabler, S
dc.identifier.name-orcidYung, R; 0000-0002-8181-027X
dc.working.doi10.7302/22744en
dc.owningcollnameInternal Medicine, Department of


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Licence for published version: Creative Commons Attribution 4.0 International
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