Disruption of Nrf2, a Key Inducer of Antioxidant Defenses, Attenuates ApoE-Mediated Atherosclerosis in Mice 英文参考文献.docVIP

下载本文档

6
0
约3.55万字
约 9页
2017-05-11 发布于上海
举报
版权申诉

Disruption of Nrf2, a Key Inducer of Antioxidant Defenses, Attenuates ApoE-Mediated Atherosclerosis in Mice 英文参考文献.doc

1、本文档共9页，可阅读全部内容。
2、原创力文档（book118）网站文档一经付费（服务费），不意味着购买了该文档的版权，仅供个人/单位学习、研究之用，不得用于商业用途，未经授权，严禁复制、发行、汇编、翻译或者网络传播等，侵权必究。
3、本站所有内容均由合作方或网友上传，本站不对文档的完整性、权威性及其观点立场正确性做任何保证或承诺！文档内容仅供研究参考，付费前请自行鉴别。如您付费，意味着您自己接受本站规则且自行承担风险，本站不退款、不进行额外附加服务；查看《如何避免下载的几个坑》。如果您已付费下载过本站文档，您可以点击这里二次下载。
4、如文档侵犯商业秘密、侵犯著作权、侵犯人身权等，请点击“版权申诉”（推荐），也可以打举报电话：400-050-0827(电话支持时间：9:00-18:30)。
5、该文档为VIP文档，如果想要下载，成为VIP会员后，下载免费。
6、成为VIP后，下载本文档将扣除1次下载权益。下载后，不支持退款、换文档。如有疑问请联系我们。
7、成为VIP后，您将拥有八大权益，权益包括：VIP文档下载权益、阅读免打扰、文档格式转换、高级专利检索、专属身份标志、高级客服、多端互通、版权登记。
8、VIP文档为合作方或网友上传，每下载1次，网站将根据用户上传文档的质量评分、类型等，对文档贡献者给予高额补贴、流量扶持。如果你也想贡献VIP文档。上传文档

Disruption of Nrf2, a Key Inducer of Antioxidant Defenses, Attenuates ApoE-Mediated Atherosclerosis in Mice 英文参考文献

DisruptionofNrf2,aKeyInducerofAntioxidant Defenses,AttenuatesApoE-MediatedAtherosclerosisin Mice ThomasE.Sussan1,JonathanJun2,RajeshThimmulappa1,DjahidaBedja3,MariaAntero1,KathleenL. Gabrielson3,VsevolodY.Polotsky2,ShyamBiswal1,2* 1DepartmentofEnvironmentalHealthSciences,BloombergSchoolofPublicHealth,JohnsHopkinsUniversity,Baltimore,Maryland,UnitedStatesofAmerica,2Division of Pulmonary and Critical Care Medicine, Department of Medicine, School of Medicine, Johns Hopkins University, Baltimore, Maryland, United States of America, 3DepartmentofMolecularandComparativePathobiology,SchoolofMedicine,JohnsHopkinsUniversity,Baltimore,Maryland,UnitedStatesofAmerica Abstract Background: Oxidative stress and inflammation are two critical factors that drive the formation of plaques in atherosclerosis. Nrf2 is a redox-sensitive transcription factor that upregulates a battery of antioxidative genes and cytoprotective enzymes that constitute the cellular response to oxidative stress. Our previous studies have shown that disruptionofNrf2inmice(Nrf22/2)causesincreasedsusceptibilitytopulmonaryemphysema,asthmaandsepsisdueto increased oxidative stress and inflammation. Here we have tested the hypothesis that disruption of Nrf2 in mice causes increasedatherosclerosis. Principal Findings: To investigate the role of Nrf2 in the development of atherosclerosis, we crossed Nrf22/2 mice with apoliporoteinE-deficient(ApoE2/2)mice.ApoE2/2andApoE2/2Nrf22/2micewerefedanatherogenicdietfor20weeks, andplaqueareawasassessedintheaortas.Surprisingly,ApoE2/2Nrf22/2miceexhibitedsignificantlysmallerplaquearea thanApoE2/2 controls(11.5%vs29.5%).ThisdecreaseinplaqueareaobservedinApoE2/2 Nrf22/2 micewasassociated withasignificantdecreaseinuptakeofmodifiedlowdensitylipoproteins(AcLDL)byisolatedmacrophagesfromApoE2/2 Nrf22/2 mice. Furthermore, atherosclerotic plaques and isolated macrophages from ApoE2/2 Nrf22/2 mice exhibited decreasedexpressionofthescavengerreceptorCD36. Conclusions:Nrf2ispro-athero