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Caveolin plays a central role in endothelial progenitor cell mobilization and homing in SDF-1-driven postischemic vasculogenesis.
Circ Res. 2006 May 12; 98(9):1219-27.CircR

Abstract

When neovascularization is triggered in ischemic tissues, angiogenesis but also (postnatal) vasculogenesis is induced, the latter requiring the mobilization of endothelial progenitor cells (EPC) from the bone marrow. Caveolin, the structural protein of caveolae, was recently reported to directly influence the angiogenic process through the regulation of the vascular endothelial growth factor (VEGF)/nitric oxide pathway. In this study, using caveolin-1 null mice (Cav(-/-)), we examined whether caveolin was also involved in the EPC recruitment in a model of ischemic hindlimb. Intravenous infusion of Sca-1(+) Lin(-) progenitor cells, but not bone marrow transplantation, rescued the defective neovascularization in Cav(-/-) mice, suggesting a defect in progenitor mobilization. The adhesion of Cav(-/-) EPC to bone marrow stromal cells indeed appeared to be resistant to the otherwise mobilizing SDF-1 (Stromal cell-Derived Factor-1) exposure because of a defect in the internalization of the SDF-1 cognate receptor CXCR4. Symmetrically, the attachment of Cav(-/-) EPC to SDF-1-presenting endothelial cells was significantly increased. Finally, EPC transduction with caveolin small interfering RNA reproduced this advantage in vitro and, importantly, led to a more extensive rescue of the ischemic hindlimb after intravenous infusion (versus sham-transfected EPC). These results underline the critical role of caveolin in ensuring the caveolae-mediated endocytosis of CXCR4, regulating both the SDF-1-mediated mobilization and peripheral homing of progenitor cells in response to ischemia. In particular, a transient reduction in caveolin expression was shown to therapeutically increase the engraftment of progenitor cells.

Authors+Show Affiliations

Unit of Pharmacology and Therapeutics, University of Louvain Medical School, Brussels, Belgium.No 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

16601228

Citation

Sbaa, Elhem, et al. "Caveolin Plays a Central Role in Endothelial Progenitor Cell Mobilization and Homing in SDF-1-driven Postischemic Vasculogenesis." Circulation Research, vol. 98, no. 9, 2006, pp. 1219-27.
Sbaa E, Dewever J, Martinive P, et al. Caveolin plays a central role in endothelial progenitor cell mobilization and homing in SDF-1-driven postischemic vasculogenesis. Circ Res. 2006;98(9):1219-27.
Sbaa, E., Dewever, J., Martinive, P., Bouzin, C., Frérart, F., Balligand, J. L., Dessy, C., & Feron, O. (2006). Caveolin plays a central role in endothelial progenitor cell mobilization and homing in SDF-1-driven postischemic vasculogenesis. Circulation Research, 98(9), 1219-27.
Sbaa E, et al. Caveolin Plays a Central Role in Endothelial Progenitor Cell Mobilization and Homing in SDF-1-driven Postischemic Vasculogenesis. Circ Res. 2006 May 12;98(9):1219-27. PubMed PMID: 16601228.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Caveolin plays a central role in endothelial progenitor cell mobilization and homing in SDF-1-driven postischemic vasculogenesis. AU - Sbaa,Elhem, AU - Dewever,Julie, AU - Martinive,Philippe, AU - Bouzin,Caroline, AU - Frérart,Françoise, AU - Balligand,Jean-Luc, AU - Dessy,Chantal, AU - Feron,Olivier, Y1 - 2006/04/06/ PY - 2006/4/8/pubmed PY - 2006/6/17/medline PY - 2006/4/8/entrez SP - 1219 EP - 27 JF - Circulation research JO - Circ Res VL - 98 IS - 9 N2 - When neovascularization is triggered in ischemic tissues, angiogenesis but also (postnatal) vasculogenesis is induced, the latter requiring the mobilization of endothelial progenitor cells (EPC) from the bone marrow. Caveolin, the structural protein of caveolae, was recently reported to directly influence the angiogenic process through the regulation of the vascular endothelial growth factor (VEGF)/nitric oxide pathway. In this study, using caveolin-1 null mice (Cav(-/-)), we examined whether caveolin was also involved in the EPC recruitment in a model of ischemic hindlimb. Intravenous infusion of Sca-1(+) Lin(-) progenitor cells, but not bone marrow transplantation, rescued the defective neovascularization in Cav(-/-) mice, suggesting a defect in progenitor mobilization. The adhesion of Cav(-/-) EPC to bone marrow stromal cells indeed appeared to be resistant to the otherwise mobilizing SDF-1 (Stromal cell-Derived Factor-1) exposure because of a defect in the internalization of the SDF-1 cognate receptor CXCR4. Symmetrically, the attachment of Cav(-/-) EPC to SDF-1-presenting endothelial cells was significantly increased. Finally, EPC transduction with caveolin small interfering RNA reproduced this advantage in vitro and, importantly, led to a more extensive rescue of the ischemic hindlimb after intravenous infusion (versus sham-transfected EPC). These results underline the critical role of caveolin in ensuring the caveolae-mediated endocytosis of CXCR4, regulating both the SDF-1-mediated mobilization and peripheral homing of progenitor cells in response to ischemia. In particular, a transient reduction in caveolin expression was shown to therapeutically increase the engraftment of progenitor cells. SN - 1524-4571 UR - https://www.unboundmedicine.com/medline/citation/16601228/Caveolin_plays_a_central_role_in_endothelial_progenitor_cell_mobilization_and_homing_in_SDF_1_driven_postischemic_vasculogenesis_ L2 - https://www.ahajournals.org/doi/10.1161/01.RES.0000220648.80170.8b?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -