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Cardiovascular Research Advance Access first published online on July 3, 2009
This version [Corrected Proof] published online on July 21, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp215
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.
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Bone marrow-derived cells do not repair endothelium in a mouse model of chronic endothelial cell dysfunction

Tashera E. Perry1,{dagger}, Minjung Song1,{dagger}, Daryl J. Despres2, Soo Mi Kim3, Hong San4, Zu-Xi Yu5, Nalini Raghavachari6, Jurgen Schnermann3, Richard O. Cannon, III1 and Donald Orlic1,*

1 Translational Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, 9000 Rockville Pike, Building 10-CRC, Room 6-3130, Bethesda, MD 20892, USA
2 Mouse Imaging Facility, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA
3 Kidney Disease Branch, National Institute of Diabetes and Digestive and Kidney Disease, National Institutes of Health, Bethesda, MD, USA
4 Genome Technology, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA
5 Pathology Core, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA
6 Gene Expression Core, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA

* Corresponding author. Tel: +1 301 402 0903; fax: +1 301 402 0888. E-mail address: dorlic{at}nhlbi.nih.gov

Aims: Bone marrow (BM)-derived endothelial progenitor cells (EPCs) in the circulation replace damaged vascular endothelium. We assessed the hypothesis that a BM transplant from healthy animals would restore normal arterial endothelium and prevent hypertension in young endothelial nitric oxide synthase-deficient (eNOS–/–) mice.

Methods and results: Radiation or busulfan-induced BM ablation in eNOS–/– mice on day 6, day 14, or day 28 was followed by a BM transplant consisting of enhanced green fluorescent protein positive (EGFP+) cells from C57BL/6J mice. Peripheral blood cell chimerism was always greater than 85% at 4 months after BM transplant. Molecular assays of heart, kidney, and liver revealed low-level chimerism in all treatment groups, consistent with residual circulating EGFP+ blood cells. When aorta, coronary, renal, hepatic, and splenic arteries in BM-transplanted eNOS–/– mice were examined by confocal microscopy, there were no EGFP- or eNOS-positive endothelial cells detected in these vessels in any of the treatment groups. Likewise, telemetry did not detect any reduction in blood pressure. Thus, no differences were observed in our measurements using several different treatment protocols.

Conclusion: We found no evidence for BM-derived EPC renewal of endothelium in this eNOS-deficient mouse model of a chronic vascular disease or in wild-type mice during postnatal growth. Hence, renewal of chronic dysfunctional endothelium and endothelial homeostasis may be dependent on resident vascular progenitor cells.

KEYWORDS Stem cells; Bone marrow transplantation; Endothelial NOS deficiency; Hypertension

Time for primary review: 29 days

{dagger} These two authors contributed equally to this study.


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