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Vascular endothelial growth factor expression in transplanted human hearts
R J Torry1, C A Labarrere, D S Torry
1Center for Reproduction and Transplantation Immunology, Methodist Hospital of Indiana, Indianapolis 46202, USA.
Transplantation
|December 27, 1995
Summary
Vascular Endothelial Growth Factor (VEGF) is expressed in transplanted hearts with microvascular fibrin and myocardial damage. VEGF expression correlates with endothelial cell activation and may play a role in thrombosis and allograft rejection.
Area of Science:
- Cardiovascular Biology
- Immunology
- Regenerative Medicine
Background:
- Vascular Endothelial Growth Factor (VEGF) is crucial for blood vessel formation.
- Its role in cardiac allografts, particularly post-transplant thrombosis, requires further investigation.
Purpose of the Study:
- To investigate the expression and localization of VEGF in transplanted human hearts.
- To correlate VEGF expression with microvascular fibrin deposition, inflammatory cell infiltration, and endothelial cell activation.
Main Methods:
- Immunocytochemistry was used to detect VEGF in 283 biopsies from 109 transplanted hearts.
- Analysis included markers for fibrin, alpha 2 plasmin-inhibitor (a2PI), macrophages, neutrophils, T cells, HLA-DR, ICAM-1, and PAL-E.
- Nested RT-PCR identified VEGF variants.
Main Results:
- VEGF immunoreactivity was absent in control hearts but significantly increased with fibrin and a2PI deposition in allografts.
- VEGF expression localized to fibrin deposits and was associated with macrophages, neutrophils, and endothelial cell activation markers (HLA-DR, ICAM-1, PAL-E).
- VEGF-positive biopsies correlated with higher serum cardiac troponin-T levels and expressed VEGF121, VEGF165, and VEGF189 variants.
Conclusions:
- Endogenous VEGF is locally expressed in cardiac allografts following vascular thrombosis and myocardial damage.
- VEGF expression is linked to endothelial cell activation and phenotypic changes in the microcirculation.
- VEGF may play a role in the pathogenesis of thrombosis and inflammation in cardiac allografts.