Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/17277
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dc.contributor.authorMarques, Francine Z-
dc.contributor.authorPrestes, Priscilla R-
dc.contributor.authorByars, Sean G-
dc.contributor.authorRitchie, Scott C-
dc.contributor.authorWürtz, Peter-
dc.contributor.authorPatel, Sheila K-
dc.contributor.authorBooth, Scott A-
dc.contributor.authorRana, Indrajeetsinh-
dc.contributor.authorMinoda, Yosuke-
dc.contributor.authorBerzins, Stuart P-
dc.contributor.authorCurl, Claire L-
dc.contributor.authorBell, James R-
dc.contributor.authorWai, Bryan-
dc.contributor.authorSrivastava, Piyush M-
dc.contributor.authorKangas, Antti J-
dc.contributor.authorSoininen, Pasi-
dc.contributor.authorRuohonen, Saku-
dc.contributor.authorKähönen, Mika-
dc.contributor.authorLehtimäki, Terho-
dc.contributor.authorRaitoharju, Emma-
dc.contributor.authorHavulinna, Aki-
dc.contributor.authorPerola, Markus-
dc.contributor.authorRaitakari, Olli-
dc.contributor.authorSalomaa, Veikko-
dc.contributor.authorAla-Korpela, Mika-
dc.contributor.authorKettunen, Johannes-
dc.contributor.authorMcGlynn, Maree-
dc.contributor.authorKelly, Jason-
dc.contributor.authorWlodek, Mary E-
dc.contributor.authorLewandowski, Paul A-
dc.contributor.authorDelbridge, Lea M-
dc.contributor.authorBurrell, Louise M-
dc.contributor.authorInouye, Michael-
dc.contributor.authorHarrap, Stephen B-
dc.contributor.authorCharchar, Fadi J-
dc.date2017-
dc.date.accessioned2018-03-22T23:32:11Z-
dc.date.available2018-03-22T23:32:11Z-
dc.date.issued2017-06-14-
dc.identifier.citationJournal of the American Heart Association 2017; 6: e005971en_US
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/17277-
dc.description.abstractCardiac hypertrophy increases the risk of developing heart failure and cardiovascular death. The neutrophil inflammatory protein, lipocalin-2 (LCN2/NGAL), is elevated in certain forms of cardiac hypertrophy and acute heart failure. However, a specific role for LCN2 in predisposition and etiology of hypertrophy and the relevant genetic determinants are unclear. Here, we defined the role of LCN2 in concentric cardiac hypertrophy in terms of pathophysiology, inflammatory expression networks, and genomic determinants. We used 3 experimental models: a polygenic model of cardiac hypertrophy and heart failure, a model of intrauterine growth restriction andLcn2-knockout mouse; cultured cardiomyocytes; and 2 human cohorts: 114 type 2 diabetes mellitus patients and 2064 healthy subjects of the YFS (Young Finns Study). In hypertrophic heart rats, cardiac and circulatingLcn2was significantly overexpressed before, during, and after development of cardiac hypertrophy and heart failure.Lcn2expression was increased in hypertrophic hearts in a model of intrauterine growth restriction, whereasLcn2-knockout mice had smaller hearts. In cultured cardiomyocytes,Lcn2activated molecular hypertrophic pathways and increased cell size, but reduced proliferation and cell numbers. Increased LCN2 was associated with cardiac hypertrophy and diastolic dysfunction in diabetes mellitus. In the YFS,LCN2expression was associated with body mass index and cardiac mass and with levels of inflammatory markers. The single-nucleotide polymorphism, rs13297295, located nearLCN2defined a significantcis-eQTL forLCN2expression. Direct effects of LCN2 on cardiomyocyte size and number and the consistent associations in experimental and human analyses reveal a central role for LCN2 in the ontogeny of cardiac hypertrophy and heart failure.en_US
dc.language.isoeng-
dc.subjectC‐reactive proteinen_US
dc.subjectGlycAen_US
dc.subjectNGALen_US
dc.subjectconcentric hypertrophyen_US
dc.subjectgene coexpression networksen_US
dc.subjecthypertrophyen_US
dc.subjectlipocalin‐2en_US
dc.subjectsystems biologyen_US
dc.titleExperimental and Human Evidence for Lipocalin-2 (Neutrophil Gelatinase-Associated Lipocalin [NGAL]) in the Development of Cardiac Hypertrophy and heart failure.en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleJournal of the American Heart Associationen_US
dc.identifier.affiliationSchool of Applied and Biomedical Sciences, Faculty of Science and Technology, Federation University Australia, Ballarat, Victoria, Australiaen_US
dc.identifier.affiliationMedicine (University of Melbourne)en_US
dc.identifier.affiliationHeart Failure Research Group, Baker Heart and Diabetes Research Institute, Melbourne, Victoria, Australiaen_US
dc.identifier.affiliationCentre for Systems Genomics, The University of Melbourne, Victoria, Australiaen_US
dc.identifier.affiliationSchool of BioSciences, The University of Melbourne, Victoria, Australiaen_US
dc.identifier.affiliationDepartment of Pathology, The University of Melbourne, Victoria, Australiaen_US
dc.identifier.affiliationComputational Medicine, Faculty of Medicine, University of Oulu and Biocenter Oulu, Oulu, Finlanden_US
dc.identifier.affiliationDepartment of Microbiology and Immunology, Peter Doherty Institute, The University of Melbourne, Victoria, Australiaen_US
dc.identifier.affiliationDepartment of Physiology, The University of Melbourne, Victoria, Australiaen_US
dc.identifier.affiliationCardiologyen_US
dc.identifier.affiliationNMR Metabolomics Laboratory, School of Pharmacy, University of Eastern Finland, Kuopio, Finlanden_US
dc.identifier.affiliationResearch Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Finlanden_US
dc.identifier.affiliationDepartment of Clinical Physiology, University of Tampere and Tampere University Hospital, Tampere, Finlanden_US
dc.identifier.affiliationFimlab Laboratories, Department of Clinical Chemistry, Pirkanmaa Hospital District, School of Medicine, University of Tampere, Finlanden_US
dc.identifier.affiliationNational Institute for Health and Welfare, Helsinki, Finlanden_US
dc.identifier.affiliationInstitute for Molecular Medicine Finland, University of Helsinki, Finlanden_US
dc.identifier.affiliationDepartment of Clinical Physiology and Nuclear Medicine, Turku University Hospital, Turku, Finlanden_US
dc.identifier.affiliationMedical Research Council Integrative Epidemiology Unit, University of Bristol, United Kingdomen_US
dc.identifier.affiliationSchool of Social and Community Medicine, University of Bristol, United Kingdomen_US
dc.identifier.affiliationSchool of Medicine, Deakin University, Waurn Ponds, Victoria, Australiaen_US
dc.identifier.affiliationDepartment of Cardiovascular Sciences, University of Leicester, United Kingdomen_US
dc.identifier.doi10.1161/JAHA.117.005971en_US
dc.type.contentTexten_US
dc.identifier.orcid0000-0003-1863-7539en_US
dc.identifier.pubmedid28615213-
dc.type.austinJournal Article-
local.name.researcherBurrell, Louise M
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptMedicine (University of Melbourne)-
crisitem.author.deptMedicine (University of Melbourne)-
crisitem.author.deptCardiology-
crisitem.author.deptGeneral Medicine-
crisitem.author.deptMedicine (University of Melbourne)-
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