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Overexpression of vascular endothelial growth factor-B in mouse heart alters cardiac lipid metabolism and induces myocardial hypertrophy

Karpanen, Terhi (författare)
Molecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Biomedicum Helsinki and Haartman Institute, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland;
Bry, Maija (författare)
Molecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Biomedicum Helsinki and Haartman Institute, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland
Ollila, Hanna M. (författare)
Molecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Biomedicum Helsinki and Haartman Institute, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland
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Seppänen-Laakso, Tuulikki (författare)
VTT Technical Research Centre of Finland, Espoo, Finland
Liimatta, Erkki (författare)
Department of Medical Biochemistry and Molecular Biology, University of Oulu, Oulu, Finland
Leskinen, Hanna (författare)
Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland
Kivelä, Riikka (författare)
Molecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Biomedicum Helsinki and Haartman Institute, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland
Helkamaa, Teemu (författare)
Institute of Biomedicine, Department of Pharmacology, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland
Merentie, Mari (författare)
A.I. Virtanen Institute, Department of Biotechnology and Molecular Medicine, University of Kuopio, Kuopio, Finland
Jeltsch, Michael (författare)
Molecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Biomedicum Helsinki and Haartman Institute, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland
Paavonen, Karri (författare)
Molecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Biomedicum Helsinki and Haartman Institute, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland
Andersson, Leif C. (författare)
Department of Pathology, Haartman Institute, University of Helsinki, Helsinki, Finland
Mervaala, Eero (författare)
Institute of Biomedicine, Department of Pharmacology, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland
Hassinen, Ilmo E. (författare)
Department of Medical Biochemistry and Molecular Biology, University of Oulu, Oulu, Finland
Ylä-Herttuala, Seppo (författare)
A.I. Virtanen Institute, Department of Biotechnology and Molecular Medicine, University of Kuopio, Kuopio, Finland
Oresic, Matej, 1967- (författare)
VTT Technical Research Centre of Finland, Espoo, Finland
Alitalo, Kari (författare)
Molecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Biomedicum Helsinki and Haartman Institute, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland
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 (creator_code:org_t)
American Heart Association, 2008
2008
Engelska.
Ingår i: Circulation Research. - : American Heart Association. - 0009-7330 .- 1524-4571. ; 103:9, s. 1018-1026
Relaterad länk:
https://urn.kb.se/re...
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https://doi.org/10.1...
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  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • Vascular endothelial growth factor (VEGF)-B is poorly angiogenic but prominently expressed in metabolically highly active tissues, including the heart. We produced mice expressing a cardiac-specific VEGF-B transgene via the alpha-myosin heavy chain promoter. Surprisingly, the hearts of the VEGF-B transgenic mice showed concentric cardiac hypertrophy without significant changes in heart function. The cardiac hypertrophy was attributable to an increased size of the cardiomyocytes. Blood capillary size was increased, whereas the number of blood vessels per cell nucleus remained unchanged. Despite the cardiac hypertrophy, the transgenic mice had lower heart rate and blood pressure than their littermates, and they responded similarly to angiotensin II-induced hypertension, confirming that the hypertrophy does not compromise heart function. Interestingly, the isolated transgenic hearts had less cardiomyocyte damage after ischemia. Significantly increased ceramide and decreased triglyceride levels were found in the transgenic hearts. This was associated with structural changes and eventual lysis of mitochondria, resulting in accumulation of intracellular vacuoles in cardiomyocytes and increased death of the transgenic mice, apparently because of mitochondrial lipotoxicity in the heart. These results suggest that VEGF-B regulates lipid metabolism, an unexpected function for an angiogenic growth factor.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Andra medicinska och farmaceutiska grundvetenskaper (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Other Basic Medicine (hsv//eng)

Nyckelord

VEGF-B
cardiac hypertrophy
cardiac metabolism
fatty acids
mitochondria

Publikations- och innehållstyp

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