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Mouse Model of Alloimmune-induced Vascular Rejection and Transplant Arteriosclerosis
Published on: May 17, 2015
Impaired endothelial progenitor cell recruitment may contribute to heart transplant microvasculopathy
Elena Osto1, Chiara Castellani, Gian Paolo Fadini
1Department of Cardiology, University of Padova, Padova, Italy.
Insights
Decreased endothelial progenitor cells (EPCs) in heart transplant patients are linked to cardiac allograft vasculopathy. Lower EPCs in circulation and allografts suggest a role in disease development.
Area of Science:
- Cardiovascular Research
- Transplantation Immunology
- Regenerative Medicine
Background:
- Cardiac allograft vasculopathy (CAV) is a primary cause of death after heart transplantation (HTx).
- Circulating progenitor cells (PCs) are implicated in the development of CAV.
- This study investigates the link between circulating PCs, their integration into cardiac allografts, and coronary microvascular function in HTx recipients.
Purpose of the Study:
- To assess the relationship between circulating progenitor cells (PCs) and their incorporation into cardiac allografts.
- To evaluate the association between circulating PCs and coronary microvascular function in heart transplant recipients.
- To explore the role of endothelial progenitor cells (EPCs) in the pathogenesis of cardiac allograft vasculopathy.
Main Methods:
- Quantified circulating progenitor cells (PCs) using flow cytometry, identifying CD34, CD133, and kinase domain receptor (KDR) surface antigens.
- Analyzed biopsy specimens using immunohistochemistry for stem cell marker c-Kit, endothelial PC (EPC) marker KDR, and CD34.
- Measured coronary flow reserve (CFR) via transthoracic echocardiography at rest and during adenosine-induced hyperemia.
Main Results:
- Patients with abnormal CFR (Group A) exhibited significantly lower counts of circulating CD34(+)KDR(+), CD133(+)KDR(+), and CD34(+)CD133(+)KDR(+) cells compared to those with normal CFR (Group B).
- EPCs in biopsy sections were reduced in Group A, showing a trend towards significance (p = 0.06).
- The number of EPCs in biopsy sections correlated with circulating CD133(+)KDR(+) and CD34(+)CD133(+)KDR(+) cells.
Conclusions:
- Endothelial progenitor cells (EPCs) are diminished in both circulation and allografts of patients with cardiac microvasculopathy.
- Impaired mobilization and engraftment of EPCs are suggested to contribute to the pathogenesis of cardiac allograft vasculopathy.
- These findings highlight a potential therapeutic target for preventing or treating CAV.
Background:
Circulating progenitor cells (PCs) may play a role in the pathogenesis of cardiac allograft vasculopathy, the leading cause of morbidity and mortality in heart transplantation (HTx). We assessed the relationship between circulating PCs and their incorporation into allografts and coronary microvascular function in HTx.
Methods:
PCs were quantified by flow cytometry on the basis of the surface expression of CD34, CD133, and kinase domain receptor (KDR) antigens. Biopsy specimens at 2 different times were examined. Immunohistochemistry for the stem cell marker c-Kit, endothelial PC (EPC) marker KDR, and CD34 was performed in serial sections in all specimens. Cells positive for each marker were counted in all specimen area sections, and the number obtained was corrected by area section. Coronary flow in the left anterior descending coronary artery was detected at rest and during intravenous adenosine by transthoracic echocardiography. Coronary flow reserve (CFR) was the ratio of hyperemic diastolic mean velocity (DMV)/resting DMV.
Results:
CFR was measured in 29 patients and was abnormal (CFR < 2) in 6 (Group A) and normal in 23 (Group B). CFR was lower in Group A (1.5 ± 0.1 vs 3.3 ± 0.8, p < 0.0001). CD34(+)KDR(+), CD133(+)KDR(+), and CD34(+)CD133(+)KDR(+) cell counts were lower in Group A (p < 0.05). EPCs in biopsy sections tended to be lower in Group A (p = 0.06) and correlated to circulating CD133(+)KDR(+) and CD34(+)CD133(+)KDR(+) (p = 0.003 and p = 0.052, respectively).
Conclusions:
EPCs are decreased in the circulation and in the allograft in patients with microvasculopathy. Defective mobilization and engraftment of EPCs may be involved in the pathogenesis of cardiac allograft vasculopathy.
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