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Endothelial progenitor cells participate in nicotine-mediated angiogenesis.
J Am Coll Cardiol. 2006 Dec 19; 48(12):2553-60.JACC

Abstract

OBJECTIVES

We aimed to determine the role of endothelial progenitor cells (EPCs) in cholinergic angiogenesis.

BACKGROUND

Recently, we provided evidence for a new angiogenic pathway mediated by endothelial nicotinic acetylcholine receptors (nAChR). Increasing evidence suggests that circulating EPCs also contribute to postnatal neovascularization by homing to sites of neovascularization, a process termed postnatal vasculogenesis. Therefore, we investigated whether nAChR activation increases mobilization and/or recruitment of EPCs to a site of angiogenesis.

METHODS

To identify EPCs from reservoirs both inside and outside of the bone marrow and to avoid the adverse effects of total body irradiation, we employed a murine parabiosis model with tie-2-LacZ FvB/N mice connected to wild-type FvB/N mice and induced unilateral hind limb ischemia in the wild-type animal.

RESULTS

Administration of nicotine increased capillary density in the ischemic hind limb, and increased soluble Kit ligand plasma levels. The effect of systemic administration was greater than that of local delivery of nicotine (45% vs. 76% increase in capillary density by comparison to vehicle control, intramuscular vs. oral administration of nicotine; p < 0.05). Ischemia-induced incorporation of EPC in the control group was rare, but was increased 5-fold by systemic administration of nicotine. Exposure to nicotine in vitro increased EPC count and EPC transmigration. Finally, systemic administration of nicotine increased EPC number in the bone marrow and spleen during hind limb ischemia.

CONCLUSIONS

Nicotine treatment increased the number of EPCs in the bone marrow and spleen, and increased their incorporation into the vasculature of ischemic tissue. Administration of nicotine increased markers of EPC mobilization. This study indicates that the known angiogenic effect of nicotine may be mediated in part by mobilization of precursor cells.

Authors+Show Affiliations

Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California 94305, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17174197

Citation

Heeschen, Christopher, et al. "Endothelial Progenitor Cells Participate in Nicotine-mediated Angiogenesis." Journal of the American College of Cardiology, vol. 48, no. 12, 2006, pp. 2553-60.
Heeschen C, Chang E, Aicher A, et al. Endothelial progenitor cells participate in nicotine-mediated angiogenesis. J Am Coll Cardiol. 2006;48(12):2553-60.
Heeschen, C., Chang, E., Aicher, A., & Cooke, J. P. (2006). Endothelial progenitor cells participate in nicotine-mediated angiogenesis. Journal of the American College of Cardiology, 48(12), 2553-60.
Heeschen C, et al. Endothelial Progenitor Cells Participate in Nicotine-mediated Angiogenesis. J Am Coll Cardiol. 2006 Dec 19;48(12):2553-60. PubMed PMID: 17174197.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Endothelial progenitor cells participate in nicotine-mediated angiogenesis. AU - Heeschen,Christopher, AU - Chang,Edwin, AU - Aicher,Alexandra, AU - Cooke,John P, Y1 - 2006/11/28/ PY - 2006/02/24/received PY - 2006/07/10/revised PY - 2006/07/24/accepted PY - 2006/12/19/pubmed PY - 2007/1/17/medline PY - 2006/12/19/entrez SP - 2553 EP - 60 JF - Journal of the American College of Cardiology JO - J Am Coll Cardiol VL - 48 IS - 12 N2 - OBJECTIVES: We aimed to determine the role of endothelial progenitor cells (EPCs) in cholinergic angiogenesis. BACKGROUND: Recently, we provided evidence for a new angiogenic pathway mediated by endothelial nicotinic acetylcholine receptors (nAChR). Increasing evidence suggests that circulating EPCs also contribute to postnatal neovascularization by homing to sites of neovascularization, a process termed postnatal vasculogenesis. Therefore, we investigated whether nAChR activation increases mobilization and/or recruitment of EPCs to a site of angiogenesis. METHODS: To identify EPCs from reservoirs both inside and outside of the bone marrow and to avoid the adverse effects of total body irradiation, we employed a murine parabiosis model with tie-2-LacZ FvB/N mice connected to wild-type FvB/N mice and induced unilateral hind limb ischemia in the wild-type animal. RESULTS: Administration of nicotine increased capillary density in the ischemic hind limb, and increased soluble Kit ligand plasma levels. The effect of systemic administration was greater than that of local delivery of nicotine (45% vs. 76% increase in capillary density by comparison to vehicle control, intramuscular vs. oral administration of nicotine; p < 0.05). Ischemia-induced incorporation of EPC in the control group was rare, but was increased 5-fold by systemic administration of nicotine. Exposure to nicotine in vitro increased EPC count and EPC transmigration. Finally, systemic administration of nicotine increased EPC number in the bone marrow and spleen during hind limb ischemia. CONCLUSIONS: Nicotine treatment increased the number of EPCs in the bone marrow and spleen, and increased their incorporation into the vasculature of ischemic tissue. Administration of nicotine increased markers of EPC mobilization. This study indicates that the known angiogenic effect of nicotine may be mediated in part by mobilization of precursor cells. SN - 1558-3597 UR - https://www.unboundmedicine.com/medline/citation/17174197/Endothelial_progenitor_cells_participate_in_nicotine_mediated_angiogenesis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0735-1097(06)02451-X DB - PRIME DP - Unbound Medicine ER -