α-MSH

α-MSH is a 13-amino acid neuropeptide obtained from the precursor proopiomelanocortin (POMC), which is a vital stress hormone of the hypothalamus/pituitary/adrenal gland (HPA) axis [1].

Five G-protein-coupled melanocortin receptors (MC1-R to MC5-R) can transmit the signaling of melanocortins including α-MSH, which can mediate the effect of α-MSH on melanogenesis, thermoregulation, pigmentation formation, food intake, energy expenditure, and fatty acid oxidation.

In α-MSH-treated human umbilical vein endothelial cells (HUVECs), the blocking either MC1-R or MC2-R restored the Nitric Oxide release by using the antibody neutralization strategy. After immunoblot analysis, the MC1-R neutralization could inhibit the α-MSH-induced endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) signaling, while MC2-R neutralization could reverse the α-MSH-induced eNOS but not iNOS signaling in HUVECs [1].

After treatment with α-MSH with or without L-Arginine for 24 h, it showed that α-MSH treatment potently interfered with the vessel development in transgenic zebrafish, L-Arginine supplementation rescued the α-MSH-induced intersegmental vessels (ISV) and restored endothelial recruitment in ISV [1].

Reference:

[1] Weng W T, Wu C S, Wang F S, et al. α-Melanocyte-Stimulating Hormone Attenuates Neovascularization by Inducing Nitric Oxide Deficiency via MC-Rs/PKA/NF-κB Signaling [J]. International Journal of Molecular Sciences. 2018, 19(12): 3823.