ArticlePloS one2011
In vivo serial MR imaging of magnetically labeled endothelial progenitor cells homing to the endothelium injured artery in mice.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 11 citations in OpenAlex.
- Determination of portal vein tumor thrombus blood supply using in vivo cellular magnetic resonance imaging in a rabbit model.Cancer management and research · 2019Article
- Perspectives: MRI of angiogenesis.Journal of magnetic resonance (San Diego, Calif. : 1997) · 2018Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEmerging evidence of histopathological analyses suggests that endothelial progenitor cells (EPCs) play an important role in vascular diseases. Neointimal hyperplasia can be reduced by intravenous transfusion of EPCs after vascular injury in mice. Therefore, it would be advantageous to develop an in vivo technique that can explore the temporal and spatial migration of EPCs homing to the damaged endothelium noninvasively. METHODOLOGY/PRINCIPAL
findingsThe left carotid common artery (LCCA) was injured by removal of endothelium with a flexible wire in Kunming mice. EPCs were collected by in vitro culture of spleen-derived mouse mononuclear cells (MNCs). EPCs labeling was carried out in vitro using Fe₂O₃-poly-L-lysine (Fe₂O₃-PLL). In vivo serial MR imaging was performed to follow-up the injured artery at different time points after intravenous transfusion of EPCs. Vessel wall areas of injured artery were computed on T₂WI. Larger MR signal voids of vessel wall on T₂WI was revealed in all 6 mice of the labeled EPC transfusion group 15 days after LCCA injury, and it was found only in 1 mouse in the unlabeled EPC transfusion group (p = 0.015). Quantitative analyses of vessel wall areas on T₂WI showed that the vessel wall areas of labeled EPC transfusion group were less than those of unlabeled EPC transfusion group and control group fifteen days after artery injury (p<0.05). Histopathological analyses confirmed accumulation and distribution of transfused EPCs at the injury site of LCCA. CONCLUSIONS/SIGNIFICANCE: These data indicate that MR imaging might be used as an in vivo method for the tracking of EPCs homing to the endothelium injured artery.
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