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Intercellular adhesion molecule-1 is upregulated in ischemic muscle, which mediates trafficking of endothelial progenitor cells.
Arterioscler Thromb Vasc Biol. 2006 May; 26(5):1066-72.AT

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.

Authors+Show Affiliations

Cardiovascular Laboratory, Clinical Research Institute, Seoul National University Hospital, Seoul, Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16497992

Citation

Yoon, Chang-Hwan, et al. "Intercellular Adhesion Molecule-1 Is Upregulated in Ischemic Muscle, Which Mediates Trafficking of Endothelial Progenitor Cells." Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 26, no. 5, 2006, pp. 1066-72.
Yoon CH, Hur J, Oh IY, et al. Intercellular adhesion molecule-1 is upregulated in ischemic muscle, which mediates trafficking of endothelial progenitor cells. Arterioscler Thromb Vasc Biol. 2006;26(5):1066-72.
Yoon, C. H., Hur, J., Oh, I. Y., Park, K. W., Kim, T. Y., Shin, J. H., Kim, J. H., Lee, C. S., Chung, J. K., Park, Y. B., & Kim, H. S. (2006). Intercellular adhesion molecule-1 is upregulated in ischemic muscle, which mediates trafficking of endothelial progenitor cells. Arteriosclerosis, Thrombosis, and Vascular Biology, 26(5), 1066-72.
Yoon CH, et al. Intercellular Adhesion Molecule-1 Is Upregulated in Ischemic Muscle, Which Mediates Trafficking of Endothelial Progenitor Cells. Arterioscler Thromb Vasc Biol. 2006;26(5):1066-72. PubMed PMID: 16497992.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Intercellular adhesion molecule-1 is upregulated in ischemic muscle, which mediates trafficking of endothelial progenitor cells. AU - Yoon,Chang-Hwan, AU - Hur,Jin, AU - Oh,Il-Young, AU - Park,Kyung-Woo, AU - Kim,Tae-Youn, AU - Shin,Jae-Hoon, AU - Kim,Ji-Hyun, AU - Lee,Choon-Soo, AU - Chung,June-Key, AU - Park,Young-Bae, AU - Kim,Hyo-Soo, Y1 - 2006/02/23/ PY - 2006/2/25/pubmed PY - 2006/5/13/medline PY - 2006/2/25/entrez SP - 1066 EP - 72 JF - Arteriosclerosis, thrombosis, and vascular biology JO - Arterioscler Thromb Vasc Biol VL - 26 IS - 5 N2 - 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. SN - 1524-4636 UR - https://www.unboundmedicine.com/medline/citation/16497992/Intercellular_adhesion_molecule_1_is_upregulated_in_ischemic_muscle_which_mediates_trafficking_of_endothelial_progenitor_cells_ L2 - https://www.ahajournals.org/doi/10.1161/01.ATV.0000215001.92941.6c?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -