β-Defensin 3 (BD3) was identified as a ligand for the melanocortin receptors (MCRs) in 2007, although the pharmacology activity of BD3 has not been clearly elucidated. Herein, it is demonstrated that human BD3 and mouse BD3 are full micromolar agonists at the MCRs. Furthermore, mouse β-defensin 1 (BD1) and human BD1 are also MCR micromolar agonists. This work identifies BD1 as an endogenous MCR ligand and clarifies the controversial role of BD3 as a micromolar agonist.
Bibliographical noteFunding Information:
This work has been supported in part by NIH Grants R01DK097838, RO1DK064250, R01DK091906, and R01DK108893 (C.H.-L.) and an NIH Postdoctoral Fellowship F32DK108402 (M.D.E.). The Haskell-Luevano laboratory is the recipient of a 2017 Wallin Neuroscience Discovery Fund Award through the University of Minnesota.