Circulating Progenitor Cells Regenerate Endothelium of Vein Graft Atherosclerosis, Which Is Diminished in ApoE-Deficient Mice
- 17 October 2003
- journal article
- research article
- Published by Wolters Kluwer Health in Circulation Research
- Vol. 93 (8) , e76-86
- https://doi.org/10.1161/01.res.0000097864.24725.60
Abstract
Previously we showed that a large number of endothelial cells in vein grafts undergo apoptosis or necrosis during the first few days followed by endothelial regeneration. In the present study, we investigated endothelial cell death and regeneration in vein grafts using transgenic mice carrying LacZ genes driven by an endothelial TIE2 promoter. When a vein fragment from TIE2-LacZ was isografted into the carotid artery of wild-type mice, the number of β-gal+ cells were reduced at 3 days and disappeared completely by 4 weeks after grafting. Conversely, β-gal+ cells were observed on the surface of vein segments donated by wild-type mice isografted into TIE2-LacZ mice at 1 week and reached confluence by 4 weeks, suggesting recipient origins of endothelial cells. Interestingly, β-gal+ cells were evenly distributed on the surface of the whole vein segment grafted into TIE2-LacZ mice, indicating a contribution of circulating progenitor cells. When wild-type veins were grafted into a chimeric mouse carrying TIE2-L...Keywords
This publication has 44 references indexed in Scilit:
- Aging, Progenitor Cell Exhaustion, and AtherosclerosisCirculation, 2003
- Mechanical Stress‐induced DNA damage and rac‐p38MAPK Signal Pathways Mediate p53‐dependent Apoptosis in Vascular Smooth Muscle CellsThe FASEB Journal, 2002
- Endothelial Healing in Vein GraftsCirculation, 2002
- Rapid Development of Vein Graft Atheroma in ApoE-Deficient MiceThe American Journal of Pathology, 2000
- Origins of circulating endothelial cells and endothelial outgrowth from bloodJournal of Clinical Investigation, 2000
- A Progress ReportArteriosclerosis, Thrombosis, and Vascular Biology, 2000
- Increased expression of heat shock protein 65 coincides with a population of infiltrating T lymphocytes in atherosclerotic lesions of rabbits specifically responding to heat shock protein 65.Journal of Clinical Investigation, 1993
- The pathogenesis of atherosclerosis: a perspective for the 1990sNature, 1993
- Spontaneous Hypercholesterolemia and Arterial Lesions in Mice Lacking Apolipoprotein EScience, 1992
- Syndromes of accelerated atherosclerosis: Role of vascular injury and smooth muscle cell proliferationJournal of the American College of Cardiology, 1990