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Adverse effects of Hif1a mutation and maternal diabetes on the offspring heart

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F18%3A00491883" target="_blank" >RIV/67985823:_____/18:00491883 - isvavai.cz</a>

  • Alternative codes found

    RIV/86652036:_____/18:00491883 RIV/00216208:11110/18:10376797 RIV/00216208:11310/18:10376797

  • Result on the web

    <a href="http://dx.doi.org/10.1186/s12933-018-0713-0" target="_blank" >http://dx.doi.org/10.1186/s12933-018-0713-0</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1186/s12933-018-0713-0" target="_blank" >10.1186/s12933-018-0713-0</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Adverse effects of Hif1a mutation and maternal diabetes on the offspring heart

  • Original language description

    Background: Epidemiological studies show that maternal diabetes predisposes offspring to cardiovascular and metabolic disorders. However, the precise mechanisms for the underlying penetrance and disease predisposition remain poorly understood. We examined whether hypoxia-inducible factor 1 alpha, in combination with exposure to a diabetic intrauterine environment, influences the function and molecular structure of the adult offspring heart. nMethods and results: In a mouse model, we demonstrated that haploinsufficient (Hif1a(+/-)) offspring from a diabetic pregnancy developed left ventricle dysfunction at 12 weeks of age, as manifested by decreased fractional shortening and structural remodeling of the myocardium. Transcriptional profiling by RNA-seq revealed significant transcriptome changes in the left ventricle of diabetes-exposed Hif1a(+/-) offspring associated with development, metabolism, apoptosis, and blood vessel physiology. In contrast, both wild type and Hif1a(+/-) offspring from diabetic pregnancies showed changes in immune system processes and inflammatory responses. Immunohistochemical analyses demonstrated that the combination of haploinsufficiency of Hifia and exposure to maternal diabetes resulted in impaired macrophage infiltration, increased levels of advanced glycation end products, and changes in vascular homeostasis in the adult offspring heart. nConclusions: Together our findings provide evidence that a global reduction in Hifia gene dosage increases predisposition of the offspring exposed to maternal diabetes to cardiac dysfunction, and also underscore Hif1a as a critical factor in the fetal programming of adult cardiovascular disease.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30105 - Physiology (including cytology)

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Others

  • Publication year

    2018

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Cardiovascular Diabetology

  • ISSN

    1475-2840

  • e-ISSN

  • Volume of the periodical

    17

  • Issue of the periodical within the volume

    MAY 12 2018

  • Country of publishing house

    GB - UNITED KINGDOM

  • Number of pages

    16

  • Pages from-to

  • UT code for WoS article

    000432264400001

  • EID of the result in the Scopus database

    2-s2.0-85046801833