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Sökning: WFRF:(Zhuge Zhengbing) > Maternal androgen e...

  • Manti, MariaKarolinska Institutet (författare)

Maternal androgen excess induces cardiac hypertrophy and left ventricular dysfunction in female mice offspring.

  • Artikel/kapitelEngelska2020

Förlag, utgivningsår, omfång ...

  • 2019-08-05
  • Oxford University Press (OUP),2020

Nummerbeteckningar

  • LIBRIS-ID:oai:gup.ub.gu.se/298028
  • https://gup.ub.gu.se/publication/298028URI
  • https://doi.org/10.1093/cvr/cvz180DOI
  • https://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-17854URI
  • http://kipublications.ki.se/Default.aspx?queryparsed=id:143122452URI

Kompletterande språkuppgifter

  • Språk:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:ref swepub-contenttype
  • Ämneskategori:art swepub-publicationtype

Anmärkningar

  • Polycystic ovary syndrome (PCOS) is a common endocrinopathy that is suggested to increase the risk for cardiovascular disease. How PCOS may lead to adverse cardiac outcomes is unclear and here we hypothesized that prenatal exposure to dihydrotestosterone (DHT) and/or maternal obesity in mice induce adverse metabolic and cardiac programming in female offspring that resemble the reproductive features of the syndrome.The maternal obese PCOS phenotype was induced in mice by chronic high-fat-high-sucrose consumption together with prenatal DHT exposure. The prenatally androgenized (PNA) female offspring displayed cardiac hypertrophy during adulthood, an outcome that was not accompanied by aberrant metabolic profile. The expression of key genes involved in cardiac hypertrophy was up-regulated in the PNA offspring, with limited or no impact of maternal obesity. Furthermore, the activity of NADPH oxidase, a major source of reactive oxygen species in the cardiovascular system, was down-regulated in the PNA offspring heart. We next explored for early transcriptional changes in the heart of newly born PNA offspring, which could account for the long-lasting changes observed in adulthood. Neonatal PNA hearts displayed an up-regulation of transcription factors involved in cardiac hypertrophic remodelling and of the calcium-handling gene, Slc8a2. Finally, to determine the specific role of androgens in cardiovascular function, female mice were continuously exposed to DHT from pre-puberty to adulthood, with or without the antiandrogen flutamide. Continuous exposure to DHT led to adverse left ventricular remodelling, and increased vasocontractile responses, while treatment with flutamide partly alleviated these effects.Taken together, our results indicate that intrauterine androgen exposure programmes long-lasting heart remodelling in female mouse offspring that is linked to left ventricular hypertrophy and highlight the potential risk of developing cardiac dysfunction in daughters of mothers with PCOS.

Ämnesord och genrebeteckningar

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Fornes, RominaKarolinska Institutet (författare)
  • Pironti, GianluigiKarolinska Institutet (författare)
  • McCann Haworth, SarahDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden (författare)
  • Zhengbing, ZhugeDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden (författare)
  • Benrick, Anna,1979Högskolan i Skövde,Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology,Institutionen för hälsa och lärande,Forskningsspecialiseringen Hälsa och Lärande,Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Sweden,Translationell medicin TRIM, Translational Medicine(Swepub:his)benb (författare)
  • Carlström, MattiasDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden (författare)
  • Andersson, DanielKarolinska Institutet (författare)
  • Stener-Victorin, ElisabetKarolinska Institutet (författare)
  • Karolinska InstitutetDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:Cardiovascular research: Oxford University Press (OUP)116:3, s. 619-6321755-32450008-6363

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