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Intercellular adhesion molecule-1 is upregulated in ischemic muscle, which mediates trafficking of endothelial progenitor cells

Cited 72 time in Web of Science Cited 77 time in Scopus
Authors
Yoon, Chang-Hwan; Hur, Jin; Oh, Il-Young; Park, Kyung-Woo; Kim, Tae-Youn; Shin, Jae-Hoon; Kim, Ji-Hyun; Lee, Choon-Soo; Chung, June-Key; Park, Young-Bae; Kim, Hyo-Soo
Issue Date
2006-02-25
Publisher
American Heart Association
Citation
Arterioscler Thromb Vasc Biol. 2006 May;26(5):1066-72. Epub 2006 Feb 23.
Keywords
AnimalsAntigens, CD18/geneticsAntigens, CD31/physiologyCell AdhesionCell MovementEndothelial Cells/*physiologyHematopoietic Stem Cells/*physiologyHindlimb/blood supplyInflammation/etiologyIntercellular Adhesion Molecule-1/*physiologyIschemia/*metabolismMiceMice, Inbred C57BLMuscle, Skeletal/*blood supplyNeovascularization, PhysiologicStem Cell Transplantation
Abstract
BACKGROUND: Trafficking of transplanted endothelial progenitor cells (EPCs) to an ischemic organ is a critical step in neovascularization. This study was performed to elucidate the molecular mechanism of EPC trafficking in terms of adhesion molecules. METHODS AND RESULTS: Using murine hindlimb ischemia model, we examined expressions of E-selectin, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and platelet-endothelial cell adhesion molecule-1 (PECAM-1) in ischemic muscle by immunofluorescence. ICAM-1 was overexpressed in ischemic muscle compared with nonischemic muscle, whereas expressions of E-selectin, VCAM-1, and PECAM-1 did not show that much difference. ICAM-1 was also upregulated by hypoxia in murine endothelial cells (ECs) as assessed by immunoblot and flow cytometry. EPCs were attached to ECs specifically through ICAM-1/beta-2 integrin interaction in vitro. When EPCs were labeled with fluorescent dye or radioisotope (Tc-99m-HMPAO) and systemically administrated in vivo, EPCs preferentially homed to ischemic muscle. By blocking ICAM-1, EPCs entrapment to ischemic limb in vivo was significantly reduced and neovascularization induced by EPC transplantation was attenuated. CONCLUSIONS: ICAM-1 is upregulated by ischemia, and this is closely associated with EPCs entrapment to ischemic limb. Our findings suggest that ICAM-1 expression might be important in regulating the process of neovascularization through its ability to recruit EPCs.
ISSN
1524-4636 (Electronic)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16497992

http://hdl.handle.net/10371/44047
DOI
https://doi.org/10.1161/01.ATV.0000215001.92941.6c
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College of Medicine/School of Medicine (의과대학/대학원)Molecular and Genomic Medicine (분자유전체의학전공)Journal Papers (저널논문_분자유전체의학전공)
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