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  • Karpanen, TerhiMolecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Biomedicum Helsinki and Haartman Institute, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland; (författare)

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

  • Artikel/kapitelEngelska2008

Förlag, utgivningsår, omfång ...

  • American Heart Association,2008
  • printrdacarrier

Nummerbeteckningar

  • LIBRIS-ID:oai:DiVA.org:oru-70924
  • https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-70924URI
  • https://doi.org/10.1161/CIRCRESAHA.108.178459DOI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

Ingår i deldatabas

Klassifikation

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

Anmärkningar

  • 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 och genrebeteckningar

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

  • Bry, MaijaMolecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Biomedicum Helsinki and Haartman Institute, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland (författare)
  • Ollila, Hanna M.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 (författare)
  • Seppänen-Laakso, TuulikkiVTT Technical Research Centre of Finland, Espoo, Finland (författare)
  • Liimatta, ErkkiDepartment of Medical Biochemistry and Molecular Biology, University of Oulu, Oulu, Finland (författare)
  • Leskinen, HannaDepartment of Pharmacology and Toxicology, University of Oulu, Oulu, Finland (författare)
  • Kivelä, RiikkaMolecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Biomedicum Helsinki and Haartman Institute, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland (författare)
  • Helkamaa, TeemuInstitute of Biomedicine, Department of Pharmacology, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland (författare)
  • Merentie, MariA.I. Virtanen Institute, Department of Biotechnology and Molecular Medicine, University of Kuopio, Kuopio, Finland (författare)
  • Jeltsch, MichaelMolecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Biomedicum Helsinki and Haartman Institute, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland (författare)
  • Paavonen, KarriMolecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Biomedicum Helsinki and Haartman Institute, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland (författare)
  • Andersson, Leif C.Department of Pathology, Haartman Institute, University of Helsinki, Helsinki, Finland (författare)
  • Mervaala, EeroInstitute of Biomedicine, Department of Pharmacology, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland (författare)
  • Hassinen, Ilmo E.Department of Medical Biochemistry and Molecular Biology, University of Oulu, Oulu, Finland (författare)
  • Ylä-Herttuala, SeppoA.I. Virtanen Institute, Department of Biotechnology and Molecular Medicine, University of Kuopio, Kuopio, Finland (författare)
  • Oresic, Matej,1967-VTT Technical Research Centre of Finland, Espoo, Finland(Swepub:oru)moc (författare)
  • Alitalo, KariMolecular/Cancer Biology Laboratory and Ludwig Institute for Cancer Research, Biomedicum Helsinki and Haartman Institute, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland (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;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 (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:Circulation Research: American Heart Association103:9, s. 1018-10260009-73301524-4571

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