Deletion of neuropeptide Y (NPY) 2 receptor in mice results in blockage of NPY-induced angiogenesis and delayed wound healing.

@article{Ekstrand2003DeletionON,
  title={Deletion of neuropeptide Y (NPY) 2 receptor in mice results in blockage of NPY-induced angiogenesis and delayed wound healing.},
  author={A. Jonas Ekstrand and Renhai Cao and Meit A. Bjorndahl and Susanne Nystrom and Ann-Cathrine Jonsson-Rylander and Hessameh Hassani and Bengt Hallberg and Margareta I. L. Nordlander and Yihai Cao},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={2003},
  volume={100 10},
  pages={6033-8}
}
Neuropeptide Y (NPY), a 36-aa peptide, is widely distributed in the brain and peripheral tissues. Whereas physiological roles of NPY as a hormoneneurotransmitter 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… CONTINUE READING
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