J Korean Med Sci.  2014 Nov;29(Suppl 3):S237-S248. 10.3346/jkms.2014.29.S3.S237.

Effect of Endogenous Bone Marrow Derived Stem Cells Induced by AMD-3100 on Expanded Ischemic Flap

Affiliations
  • 1Department of Plastic & Reconstructive Surgery, Kangnam Sacred Heart Hospital, Hallym University Medical Center, Halllym University College of Medicine, Seoul, Korea. hiisunj@gmail.com
  • 2Department of Plastic and Reconstructive Surgery, Institute for Human Tissue Restoration, Yonsei University College of Medicine, Seoul, Korea.
  • 3Department of Plastic and Reconstructive Surgery, Eulji General Hospital, Eulji University School of Medicine, Seoul, Korea.
  • 4Departments of Otorhinolaryngology, Yonsei University College of Medicine, Seoul, Korea.
  • 5Departments of Pharmacology, Yonsei University College of Medicine, Seoul, Korea.

Abstract

The purpose of this study was to devise an expanded ischemic flap model and to investigate the role of AMD-3100 (Plerixafor, chemokine receptor 4 inhibitor) in this model by confirming its effect on mobilization of stem cells from the bone marrow. Male Sprague-Dawley rats were used as an animal research model. The mobilization of stem cells from the bone marrow was confirmed in the AMD-3100-treated group. The fractions of endothelial progenitor cells (EPC) and the vascular endothelial growth factor receptor (VEGFR) 2+ cells in the peripheral blood were increased in groups treated with AMD-3100. The expression of vascular endothelial growth factor (VEGF) was increased in response to expansion or AMD injection. The expression of stromal cell derived factor (SDF)-1 and VEGFR2 were increased only in unexpanded flap treated with AMD-3100. Treatment with AMD-3100 increased both the number and area of blood vessels. However, there were no statistically significant differences in the survival area or physiologic microcirculation in rats from the other groups. This endogenous neovascularization induced by AMD-3100 may be a result of the increase in both the area and number of vessels, as well as paracrine augmentation of the expression of VEGF and EPCs. However, the presence of a tissue expander under the flap could block the neovascularization between the flap and the recipient regardless of AMD-3100 treatment and expansion.

Keyword

Endothelial Progenitor Cell; Hematopoietic Stem Cell; Tissue Expansion; Ischemic Flap; AMD-3100; CXCR4 Inhibitor; Plerixafor

MeSH Terms

Animals
Anti-HIV Agents/pharmacology
Bone Marrow Cells/cytology
Chemokine CXCL12/biosynthesis
Endothelial Progenitor Cells/*cytology
Hematopoietic Stem Cells/*cytology
Heterocyclic Compounds/*pharmacology
Hypoxia-Inducible Factor 1, alpha Subunit/metabolism
Male
Neovascularization, Physiologic
Nitric Oxide Synthase Type III/metabolism
Rats
Rats, Sprague-Dawley
Receptors, CXCR4/antagonists & inhibitors
Surgical Flaps/*blood supply/surgery
Tissue Expansion/*methods
Vascular Endothelial Growth Factor A/biosynthesis
Vascular Endothelial Growth Factor Receptor-2/biosynthesis/metabolism
Anti-HIV Agents
Chemokine CXCL12
Heterocyclic Compounds
Hypoxia-Inducible Factor 1, alpha Subunit
Receptors, CXCR4
Vascular Endothelial Growth Factor A
Nitric Oxide Synthase Type III
Vascular Endothelial Growth Factor Receptor-2
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