The majority of the human cells co-expressed CD45 (Figure (Figure4D)4D) while ��2m/CD31 double positive human cells were rare and not integrated in the epithelium of large caliber vessels (Figure (Figure4H4H). Figure 4 Human engraftment in the heart of NOD/SCID ��2m null mice with AMI four weeks after transplantation of ALDHhi Lin- sorted human UCB cells. NOD/SCID ��2m full report null mice with AMI were transplanted with ALDHhiLin- sorted human UCB cells. The lineage … Functional recovery We have previously shown that the initial infarct size in the murine AMI model is critical for the disease progression and late infarct size[20]. Thus, animals that only receive a small infarct recover easily from injury to levels comparable to sham operated controls.

Stratifying the mice based on the day 0 infarct size in the present study did not, however, influence the interpretation of the data and all transplanted animals were included in the final evaluation. NOD/SCID ��2m null mice with AMI were transplanted with ALDHloLin- (Figure (Figure55 – Red square) or ALDHhiLin- (Figure (Figure55 – Green triangle) sorted human UCB cells or PBS (Figure (Figure55 – Blue diamond). Serial echocardiographic images were recorded for all treatment groups (PBS, ALDHloLin-, and ALDHhiLin-) on the day following surgery (day 0) and again at one and four weeks post transplantation. All treatment groups had similar sized infarcts at the time of transplantation, as evident from day 0 SWMSI. There was no improved cardiac function at the experimental end point.

At four weeks, we thus found no significant difference in EF, LV-EDV, LV-ESV or SWMSI between any of the treatment groups (Figure (Figure55). Figure 5 Cardiac function of NOD/SCID ��2m null mice with AMI four weeks after transplantation of ALDHlo Lin- or ALDHhi Lin- sorted human UCB cells or PBS. NOD/SCID ��2m null mice with AMI were transplanted with ALDHloLin- (Red square) or ALDHhi … Vascular density We analyzed whether the transplanted cells promoted re-vascularization of the infarcted tissue by host endothelial cells. Sections were stained with a murine-specific CD31 endothelial antibody and we evaluated the mean vascular density in the infarcted tissue sub-served by the infarct related artery normalized to the ��m2 tissue analyzed. CD31 is expressed on platelets and a number of hematopoietic cell types that infiltrate infarcted tissue including macrophages, neutrophils, and NK cells[24].

To avoid the potential inclusion of non-endothelial cell types (Figure (Figure6,6, open arrows) in the estimation of vascular density, we only counted CD31 positive structures with a well defined tubular morphology or Brefeldin_A an open lumen, or structures with a linear extension equal to or larger than 50 ��m (Figure (Figure6,6, solid arrows).