Crossref journal-article
Proceedings of the National Academy of Sciences
Proceedings of the National Academy of Sciences (341)
Abstract

Neuropeptide Y (NPY), a 36-aa peptide, is widely distributed in the brain and peripheral tissues. Whereas physiological roles of NPY as a hormone/neurotransmitter have been well studied, little is known about its other peripheral functions. Here, we report that NPY acts as a potent angiogenic factor in vivo using the mouse corneal micropocket and the chick chorioallantoic membrane (CAM) assays. Unlike vascular endothelial growth factor (VEGF), microvessels induced by NPY had distinct vascular tree-like structures showing vasodilation. This angiogenic pattern was similar to that induced by fibroblast growth factor-2, and the angiogenic response was dose-dependent. In the developing chick embryo, NPY stimulated vascular sprouting from preexisting blood vessels. When [Leu 31 Pro 34 ]NPY, a NPY-based analogue lacking high affinity for the NPY Y 2 receptor but capable of stimulating both Y 1 and Y 5 receptors, was used in the corneal model, no angiogenic response could be detected. In addition, NPY failed to induce angiogenesis in Y 2 receptor-null mice, suggesting that this NPY receptor subtype was mediating the angiogenic signal. In support of this finding, the Y 2 receptor, but not Y 1 , Y 4 , or Y 5 receptors, was found to be widely expressed in newly formed blood vessels. Further, a delay of skin wound healing with reduced neovascularization was found in Y 2 receptor-null mice. These data demonstrate that NPY may play an important role in the regulation of angiogenesis and angiogenesis-dependent tissue repair.

Bibliography

Ekstrand, A. J., Cao, R., Björndahl, M., Nyström, S., Jönsson-Rylander, A.-C., Hassani, H., Hallberg, B., Nordlander, M., & Cao, Y. (2003). Deletion of neuropeptide Y (NPY) 2 receptor in mice results in blockage of NPY-induced angiogenesis and delayed wound healing. Proceedings of the National Academy of Sciences, 100(10), 6033–6038.

Authors 9
  1. A. Jonas Ekstrand (first)
  2. Renhai Cao (additional)
  3. Meit Björndahl (additional)
  4. Susanne Nyström (additional)
  5. Ann-Cathrine Jönsson-Rylander (additional)
  6. Hessameh Hassani (additional)
  7. Bengt Hallberg (additional)
  8. Margareta Nordlander (additional)
  9. Yihai Cao (additional)
Dates
Type When
Created 22 years, 3 months ago (May 13, 2003, 2:28 p.m.)
Deposited 3 years, 4 months ago (April 12, 2022, 8:39 p.m.)
Indexed 1 month, 3 weeks ago (July 4, 2025, 1:33 a.m.)
Issued 22 years, 3 months ago (May 2, 2003)
Published 22 years, 3 months ago (May 2, 2003)
Published Online 22 years, 3 months ago (May 2, 2003)
Published Print 22 years, 3 months ago (May 13, 2003)
Funders 0

None

@article{Ekstrand_2003, title={Deletion of neuropeptide Y (NPY) 2 receptor in mice results in blockage of NPY-induced angiogenesis and delayed wound healing}, volume={100}, ISSN={1091-6490}, url={http://dx.doi.org/10.1073/pnas.1135965100}, DOI={10.1073/pnas.1135965100}, number={10}, journal={Proceedings of the National Academy of Sciences}, publisher={Proceedings of the National Academy of Sciences}, author={Ekstrand, A. Jonas and Cao, Renhai and Björndahl, Meit and Nyström, Susanne and Jönsson-Rylander, Ann-Cathrine and Hassani, Hessameh and Hallberg, Bengt and Nordlander, Margareta and Cao, Yihai}, year={2003}, month=may, pages={6033–6038} }