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Upregulated placenta growth factor expression in human myocardium is associated with cardiomyocyte damage
Author(s) -
Torry Ronald J.,
Labarrere Carlos A.,
Baldridge Lee Ann,
Miller Steven J.,
Torry Donald S.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.644.1
Subject(s) - fibrin , medicine , placental growth factor , downregulation and upregulation , messenger rna , transplantation , pathology , biomarker , andrology , extracellular matrix , immunology , biology , microbiology and biotechnology , gene , vascular endothelial growth factor , biochemistry , vegf receptors
The usefulness of plasma PlGF as a biomarker of acute coronary syndrome patient outcomes has been described, however little is known regarding its expression and localization in human myocardium. Right endomyocardial biopsies were obtained from donor hearts and cardiac allograft recipients. Samples were grouped according to the presence or absence of myocardial fibrin and changes in PlGF mRNA expression, protein localization, cellular infiltrates, cardiac Tn‐I, time since transplant and ISHLT rejection grades were compared between groups. Biopsies (n = 7) with fibrin expressed 1.8‐fold more PlGF mRNA than biopsies without fibrin (n=10; p < 0.03). PlGF protein was localized in cardiomyocytes, extracellular matrix and microvessels in areas of fibrin deposition and not in fibrin‐negative areas. Fibrin‐positive biopsies were also associated with increased cellular infiltrates (p < 0.05) and elevated cardiac Tn‐I titers (p < 0.03). There was no correlation between PlGF mRNA expression and degree of macrophage, T‐cell, or neutrophil infiltrates or rejection grade. PlGF mRNA expression decreased with time since transplantation (R = ‐ 0.792; p < 0.001). Our results show human myocardium expresses PlGF mRNA/protein and its expression increases with cellular and biochemical indices of myocyte damage. These data provide new support that endogenous PlGF could promote cardiac healing. Support: R01‐HD36830 (DT)