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      Upregulation of VEGF-A without angiogenesis in a mouse model of dilated cardiomyopathy caused by mitochondrial dysfunction.

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          Abstract

          Angiogenesis is implicated in a variety of human pathologies and may also play a role in the progression of heart failure. We have studied the expression of members of the vascular endothelial growth factor (VEGF) and the angiopoietin families and their receptors in mice lacking the mitochondrial transcription factor A. These mice lack functional respiratory chain activity in their myocytes and develop dilated cardiomyopathy (DCM) postnatally. We studied the hearts of the knockout mice by in situ hybridization, Western blotting analysis, and immunohistochemistry. VEGF-A mRNA and protein levels were elevated in the myocardium of the knockouts. Levels of the hypoxia inducible transcription factor 1 alpha (HIF1 alpha) and of glyceraldehyde-3-phosphate dehydrogenase transcripts were also increased, whereas those of angiopoietin-1 and -2 were reduced. Despite the striking upregulation of VEGF-A, there was no increase in capillary density in the knockout hearts. This study suggests that a disturbance in angiogenesis may contribute to the pathogenesis of DCM.

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          Author and article information

          Journal
          J. Histochem. Cytochem.
          The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
          SAGE Publications
          0022-1554
          0022-1554
          Jul 2002
          : 50
          : 7
          Affiliations
          [1 ] Department of Molecular Medicine, Karolinska Institutet, Stockholm, Sweden. emma.tham@cmm.ki.se
          Article
          10.1177/002215540205000707
          12070272
          8acfd6af-2b56-4aa4-9176-02f671921331
          History

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