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

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dc.contributor.authorYoon, Chang-Hwan-
dc.contributor.authorHur, Jin-
dc.contributor.authorOh, Il-Young-
dc.contributor.authorPark, Kyung-Woo-
dc.contributor.authorKim, Tae-Youn-
dc.contributor.authorShin, Jae-Hoon-
dc.contributor.authorKim, Ji-Hyun-
dc.contributor.authorLee, Choon-Soo-
dc.contributor.authorChung, June-Key-
dc.contributor.authorPark, Young-Bae-
dc.contributor.authorKim, Hyo-Soo-
dc.date.accessioned2010-01-25T14:16:06Z-
dc.date.available2010-01-25T14:16:06Z-
dc.date.issued2006-02-25-
dc.identifier.citationArterioscler Thromb Vasc Biol. 2006 May;26(5):1066-72. Epub 2006 Feb 23.en
dc.identifier.issn1524-4636 (Electronic)-
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16497992-
dc.identifier.urihttps://hdl.handle.net/10371/44047-
dc.description.abstractBACKGROUND: 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.en
dc.language.isoenen
dc.publisherAmerican Heart Associationen
dc.subjectAnimalsen
dc.subjectAntigens, CD18/geneticsen
dc.subjectAntigens, CD31/physiologyen
dc.subjectCell Adhesionen
dc.subjectCell Movementen
dc.subjectEndothelial Cells/*physiologyen
dc.subjectHematopoietic Stem Cells/*physiologyen
dc.subjectHindlimb/blood supplyen
dc.subjectInflammation/etiologyen
dc.subjectIntercellular Adhesion Molecule-1/*physiologyen
dc.subjectIschemia/*metabolismen
dc.subjectMiceen
dc.subjectMice, Inbred C57BLen
dc.subjectMuscle, Skeletal/*blood supplyen
dc.subjectNeovascularization, Physiologicen
dc.subjectStem Cell Transplantationen
dc.titleIntercellular adhesion molecule-1 is upregulated in ischemic muscle, which mediates trafficking of endothelial progenitor cellsen
dc.typeArticleen
dc.contributor.AlternativeAuthor윤창환-
dc.contributor.AlternativeAuthor허진-
dc.contributor.AlternativeAuthor오일영-
dc.contributor.AlternativeAuthor박경우-
dc.contributor.AlternativeAuthor김태윤-
dc.contributor.AlternativeAuthor신재훈-
dc.contributor.AlternativeAuthor김지현-
dc.contributor.AlternativeAuthor이춘수-
dc.contributor.AlternativeAuthor정준기-
dc.contributor.AlternativeAuthor박영배-
dc.contributor.AlternativeAuthor김효수-
dc.identifier.doi10.1161/01.ATV.0000215001.92941.6c-
Appears in Collections:
College of Medicine/School of Medicine (의과대학/대학원)Molecular and Genomic Medicine (분자유전체의학전공)Journal Papers (저널논문_분자유전체의학전공)
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