Abstract 1041: Vascular Leukocytes: Novel Contributors to Bone-Marrow Derived Cardiac Neovascularization
Thus far there has been no proof that cells of pure hematopoietic origin contribute to cardiac neovascularization. METHODS Mice underwent sham surgery or induction of myocardial infarction (MI) by ligation of the left anterior descending coronary artery. At 1, 4, 17 and 14 days after MI, hearts were dissected into healthy (=control) and MI areas. After homogenization, flow cytometry was performed. Further analysis consisted of real time PCR, immunohistochemistry (IHC) and two photon laser scanning microscopy (TPLSM) in separate groups at the same time points. RESULTS After MI leukocytes (CD45+ cells) expressing the canonical endothelial marker VE-Cadherin first appeared in the healthy (control) area and subsequently in the MI area (see fig⇓.). We call these cells vascular leukocytes (VLC) and 7 days post-MI 50% expressed murine CD11c, a dendritic cell (DC) marker. VLC were virtually absent after sham. The appearance of VLC in the MI area coincided with increased vascularization and expression of the angiogenic markers CD13 and CD105 on the endothelium. IHC and TPLSM confirmed co-localization of VLC with CD13 and CD31 on endothelium in the MI area. CONCLUSIONS For the first time we show the contribution of pure hematopoietic cells to cardiac angiogenesis and their ability to acquire an endothelial phenotype indicating a thus far unrecognized plasticity of these cells. The high proportion of DC indicates a previously unnoticed role of immune cells in cardiac neovascularization.