These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Depressed expression of angiogenic growth factors in the subacute phase of myocardial ischemia: a mechanism behind the remodeling plateau?
    Author: Siddiqui AJ, Fischer H, Widegren U, Grinnemo KH, Hao X, Månsson-Broberg A, Sylvén C, Gustafsson T.
    Journal: Coron Artery Dis; 2010 Mar; 21(2):65-71. PubMed ID: 20016374.
    Abstract:
    BACKGROUND AND AIMS: To investigate whether, in the subacute phase of acute myocardial infarction, in the peri-infarcted area the expressions of the vascular endothelial growth factor (VEGF-A) and angiopoietin (Ang) ligand receptors are depressed, and whether overexpression of these angiogens counteracts a downregulation of myocardial function. METHODS: Acute myocardial infarction was induced by left anterior descending artery ligation and overexpression through injection of human VEGF-A165 and Ang-1 plasmids. The capillary and arteriolar densities, Akt-1 phosphorylation and citrate synthase activity were measured concurrent with the expression of VEGF-A, VEGFR1 and R2, Ang-1, Ang-2 and Tie-2. RESULTS: One day after AMI, VEGR-2 was unchanged but all other measured factors in the two families were upregulated. After day 2, the Ang-2 expression increased but other measured factors decreased. After gene transfer, the vascular supply, Akt phosphorylation and citrate synthase activity were higher in the peri-infarcted area, where also the endogenous angiogenic growth factor expressions were increased. CONCLUSION: A rapid decrease in angiogenic stimulating factors occurs in the subacute phase of AMI and is related to a progressive decrease in myocardial contraction. A negative consequence of such a circuit is a successive reduction in the vascular supply and contractility in areas with reduced perfusion. These negative adaptations can be counteracted by angiogen overexpression.
    [Abstract] [Full Text] [Related] [New Search]