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Chronic hypoxia during development does not trigger pathologic remodeling of the chicken embryonic heart but reduces cardiomyocyte number
Linköping University, Department of Physics, Chemistry and Biology, Biology. Linköping University, Faculty of Science & Engineering.
Linköping University, Department of Physics, Chemistry and Biology, Biology. Linköping University, The Institute of Technology.
Linköping University, Department of Physics, Chemistry and Biology, Theoretical Biology. Linköping University, Faculty of Science & Engineering.ORCID iD: 0000-0001-7856-2925
Linköping University, Department of Physics, Chemistry and Biology, Biology. Linköping University, Faculty of Science & Engineering.
2015 (English)In: American Journal of Physiology. Regulatory Integrative and Comparative Physiology, ISSN 0363-6119, E-ISSN 1522-1490, Vol. 309, no 10, R1204-R1214 p.Article in journal (Refereed) PublishedText
Abstract [en]

Fetal growth restriction programs an increased risk of cardiovascular disease in adulthood, but the actual mechanisms of this developmental programming are not fully understood. Previous studies in mammalian models suggest that hearts of growth-restricted fetuses have reduced cardiomyocyte number due to reduced proliferation and premature cardiomyocyte maturation. Chicken embryos incubated under chronic hypoxia are also growth-restricted, have smaller hearts, and show signs of cardiac insufficiency posthatching. The aim of the present study was to investigate how chronic hypoxia (14% O-2) during development affects cardiomyocyte mass and how myocardial structure is altered. Hypoxic incubation reproduced the well-characterized embryonic growth restriction and an increased ventricle-to-body mass ratio (at E11, E15, E17, and E19) with reduced absolute heart mass only at E19. Cell density, apoptosis, and cardiomyocyte size were insensitive to hypoxia at E15 and E19, and no signs of ventricular wall remodeling or myocardial fibrosis were detected. Bayesian modeling provided strong support for hypoxia affecting absolute mass and proliferation rates at E15, indicating that the growth impairment, at least partly, occurs earlier in development. Neither E15 nor E19 hearts contained binucleated cardiomyocytes, indicating that fetal hypoxia does not trigger early maturation of cardiomyocytes in the chicken, which contrasts with previous results from hypoxic rat pups. In conclusion, prenatal hypoxia in the chick embryo results in a reduction in the number of cardiomyocytes without inducing ventricular remodeling, cell hypertrophy, or premature cardiomyocyte maturation.

Place, publisher, year, edition, pages
AMER PHYSIOLOGICAL SOC , 2015. Vol. 309, no 10, R1204-R1214 p.
Keyword [en]
prenatal hypoxia; cardiomyocyte endowment; heart growth; hyperplasia; hypertrophy
National Category
Biological Sciences
Identifiers
URN: urn:nbn:se:liu:diva-123806DOI: 10.1152/ajpregu.00499.2014ISI: 000365878700002PubMedID: 26423711OAI: oai:DiVA.org:liu-123806DiVA: diva2:892916
Note

Funding Agencies|FORMAS Centre of Excellence in Animal Welfare Science; Linkoping university

Available from: 2016-01-11 Created: 2016-01-11 Last updated: 2016-08-31

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