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B-type natriuretic peptide enhances vasculogenesis by promoting number and functional properties of early endothelial progenitor cells.
Tissue Eng Part A. 2009 Sep; 15(9):2741-9.TE

Abstract

OBJECTIVE

To test the hypothesis that B-type natriuretic peptide (BNP) acts as a potent vasculogenic agent by enhancing the number, proliferation, adhesion, and migration of endothelial progenitor cells (EPCs).

BACKGROUND

BNP is a neurohormonal peptide that predicts outcome and used for treatment in chronic heart failure patients. It has been shown to promote angiogenesis in experimental animals. EPCs have been demonstrated to contribute to postnatal angiogenesis and vasculogenesis.

METHODS

The number of EPC colony forming units (CFU) and levels of N-terminal ProBNP were assayed in patients with severe, yet controlled, New York Heart Association (NYHA) II-IV heart failure. The in vitro effects of BNP on early EPC-CFU numbers, proliferation, migration, adhesive, and vascular tube formation capacities were studied using human and murine systems. The effects of in vivo BNP administration on Sca-1/Flk-1 progenitors and on vasculogenesis in the hindlimb ischemia model were then assayed in wild-type mice.

RESULTS

A significant correlation was found between circulating N-terminal ProBNP levels and EPC-CFU numbers. We observed a dose-dependent effect of BNP on the numbers of CFU and proliferation capacity of human EPCs as well as on their adhesive, migratory, and tube formation properties, in vitro. Systemic BNP administration to mice led to a significant increase in bone marrow Sca-1/Flk-1 EPCs and improvement in blood flow and capillary density in the ischemic limbs of mice.

CONCLUSIONS

BNP promotes vessel growth by increasing the number of endothelial progenitors and enhancing their functional properties. These provasculogenic properties of BNP could account for some of its beneficial effects in chronic heart failure patients and may be harnessed for the purpose of improving collateral formation in ischemic subjects.

Authors+Show Affiliations

Department of Cardiology, Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.No 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

Language

eng

PubMed ID

19275472

Citation

Shmilovich, Haim, et al. "B-type Natriuretic Peptide Enhances Vasculogenesis By Promoting Number and Functional Properties of Early Endothelial Progenitor Cells." Tissue Engineering. Part A, vol. 15, no. 9, 2009, pp. 2741-9.
Shmilovich H, Ben-Shoshan J, Tal R, et al. B-type natriuretic peptide enhances vasculogenesis by promoting number and functional properties of early endothelial progenitor cells. Tissue Eng Part A. 2009;15(9):2741-9.
Shmilovich, H., Ben-Shoshan, J., Tal, R., Afek, A., Barshack, I., Maysel-Auslander, S., Harats, D., Keren, G., & George, J. (2009). B-type natriuretic peptide enhances vasculogenesis by promoting number and functional properties of early endothelial progenitor cells. Tissue Engineering. Part A, 15(9), 2741-9. https://doi.org/10.1089/ten.TEA.2008.0414
Shmilovich H, et al. B-type Natriuretic Peptide Enhances Vasculogenesis By Promoting Number and Functional Properties of Early Endothelial Progenitor Cells. Tissue Eng Part A. 2009;15(9):2741-9. PubMed PMID: 19275472.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - B-type natriuretic peptide enhances vasculogenesis by promoting number and functional properties of early endothelial progenitor cells. AU - Shmilovich,Haim, AU - Ben-Shoshan,Jeremy, AU - Tal,Reshef, AU - Afek,Arnon, AU - Barshack,Iris, AU - Maysel-Auslander,Sofia, AU - Harats,Dror, AU - Keren,Gad, AU - George,Jacob, PY - 2009/3/12/entrez PY - 2009/3/12/pubmed PY - 2009/10/29/medline SP - 2741 EP - 9 JF - Tissue engineering. Part A JO - Tissue Eng Part A VL - 15 IS - 9 N2 - OBJECTIVE: To test the hypothesis that B-type natriuretic peptide (BNP) acts as a potent vasculogenic agent by enhancing the number, proliferation, adhesion, and migration of endothelial progenitor cells (EPCs). BACKGROUND: BNP is a neurohormonal peptide that predicts outcome and used for treatment in chronic heart failure patients. It has been shown to promote angiogenesis in experimental animals. EPCs have been demonstrated to contribute to postnatal angiogenesis and vasculogenesis. METHODS: The number of EPC colony forming units (CFU) and levels of N-terminal ProBNP were assayed in patients with severe, yet controlled, New York Heart Association (NYHA) II-IV heart failure. The in vitro effects of BNP on early EPC-CFU numbers, proliferation, migration, adhesive, and vascular tube formation capacities were studied using human and murine systems. The effects of in vivo BNP administration on Sca-1/Flk-1 progenitors and on vasculogenesis in the hindlimb ischemia model were then assayed in wild-type mice. RESULTS: A significant correlation was found between circulating N-terminal ProBNP levels and EPC-CFU numbers. We observed a dose-dependent effect of BNP on the numbers of CFU and proliferation capacity of human EPCs as well as on their adhesive, migratory, and tube formation properties, in vitro. Systemic BNP administration to mice led to a significant increase in bone marrow Sca-1/Flk-1 EPCs and improvement in blood flow and capillary density in the ischemic limbs of mice. CONCLUSIONS: BNP promotes vessel growth by increasing the number of endothelial progenitors and enhancing their functional properties. These provasculogenic properties of BNP could account for some of its beneficial effects in chronic heart failure patients and may be harnessed for the purpose of improving collateral formation in ischemic subjects. SN - 1937-335X UR - https://www.unboundmedicine.com/medline/citation/19275472/B_type_natriuretic_peptide_enhances_vasculogenesis_by_promoting_number_and_functional_properties_of_early_endothelial_progenitor_cells_ L2 - https://www.liebertpub.com/doi/10.1089/ten.TEA.2008.0414?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -