The DOI matches its Crossref record; 36 of the 36 references it cites were found in a registry or an index.
Intravenous Transfusion of Endothelial Progenitor Cells Reduces Neointima Formation After Vascular Injury
Open accessAbstract
Endothelial cell damage is one important pathophysiological step of atherosclerosis and restenosis after angioplasty. Accelerated reendothelialization impairs neointima formation. We evaluated the role of intravenously transfused endothelial progenitor cells (EPCs) on reendothelialization and neointima formation in a mouse model of arterial injury. Spleen-derived mouse mononuclear cells (MNCs) were cultured in endothelial basal medium. A total of 91.8±3.2% of adherent cells showed uptake of acetylated low-density lipoprotein (Dil-Ac-LDL) and lectin binding after 4 days. Immunostaining and long-term cultures confirmed the endothelial progenitor phenotype. To determine the effect of stem cell transfusion on reendothelialization, mice received either fluorescent-labeled spleen-derived MNCs or in vitro differentiated EPCs intravenously after endothelial injury of the carotid artery. Transfused cells were strictly restricted to the injury site, and lectin binding confirmed the endothelial phenotype. Homing of transfused cells to the site of injury was only detectable in splenectomized mice. Cell transfusion caused enhanced reendothelialization associated with a reduction of neointima formation. Systemically applied spleen-derived MNCs and EPCs home to the site of vascular injury, resulting in an enhanced reendothelialization associated with decreased neointima formation. These results allow novel insights in stem cell biology and provide additional information for the treatment of vascular dysfunction and prevention of restenosis after angioplasty. The full text of this article is available online at http://www.circresaha.org.
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Cites
Isolation of Putative Progenitor Endothelial Cells for Angiogenesis
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Bone marrow cells regenerate infarcted myocardium
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Circulating endothelial progenitor cells, vascular function, and cardiovascular risk
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Mobilized bone marrow cells repair the infarcted heart, improving function and survival
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Cited by
Endothelial Progenitor Cells: Characterization and Role in Vascular Biology
Urbich, C., & Dimmeler, S. (2004) · Circulation Research · doi:10.1161/01.res.0000137877.89448.78 · Cited by 2,369
Circulating endothelial progenitor cells and cardiovascular outcomes
Werner, N., Kosiol, S., Schiegl, T., Ahlers, P., Walenta, K., Link, A., Böhm, M., & Nickenig, G. (2005) · New England Journal of Medicine · doi:10.1056/nejmoa043814 · Cited by 2,048
Self-citationExercise is the real polypill.
Fiuza-Luces, C., Garatachea, N., Berger, N. A., & Lucia, A. (2013) · Physiology · doi:10.1152/physiol.00019.2013 · Cited by 791
Endothelial and Antithrombotic Actions of HDL
Mineo, C., Deguchi, H., Griffin, J. H., & Shaul, P. W. (2006) · Circulation Research · doi:10.1161/01.res.0000225982.01988.93 · Cited by 655
Hemodialysis Vascular Access Dysfunction: A Cellular and Molecular Viewpoint
Roy-Chaudhury, P., Sukhatme, V. P., & Cheung, A. K. (2006) · Journal of the American Society of Nephrology · doi:10.1681/asn.2005050615 · Cited by 584
Metadata
- Authors
- Werner, N., Junk, S., Laufs, U., Link, A., Walenta, K., Böhm, M., & Nickenig, G.
- Venue
- Circulation Research
- Published
- 2003-07-25
- Volume
- 93
- Issue
- 2
- Pages
- e17-24
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2170579826
- Cited by
- 694
- References
- 36
- FWCI
- 12.65
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Werner, N., Junk, S., Laufs, U., Link, A., Walenta, K., Böhm, M., & Nickenig, G. (2003). Intravenous Transfusion of Endothelial Progenitor Cells Reduces Neointima Formation After Vascular Injury. Circulation Research. https://doi.org/10.1161/01.res.0000083812.30141.74
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.