Whitening effect of novel peptide mixture by regulating melanosome biogenesis, transfer and degradation

Abstract

Peptides are short chain of amino acids linked by peptide bonds. They are widely used as effective and biocompatible active ingredients in cosmetic industry. In this study, we developed novel peptide mixture and identified its anti-pigmentation effect on melanocytes and keratinocytes. Our results revealed that peptide mixture inhibited melanosome biogenesis through the regulation of microphthalmia-associated transcription factor, a key factor of melanogenesis in melanocytes. And we observed that peptide mixture inhibited melanosome uptake through the reduction of protease-activated receptor 2, a phagocytosis-related receptor in keratinocytes. Furthermore, peptide mixture activated autophagy system resulting in degradation of transferred melanosomes in keratinocytes. The anti-pigmentation effect of multi-targeting peptide mixture was assessed in a human skin equivalent model (MelanoDerm). Melanin contents in epidermal layer were significantly decreased by topical treatment of peptide mixture, suggesting that it can be applied as a novel cosmetics material having a whitening function.

Neurog1-Derived Peptides RMNE1 and DualPep-Shine Penetrate the Skin and Inhibit Melanin Synthesis by Regulating MITF Transcription

“…As alternative whitening agents, peptides have been tested for their efficacy in regulating skin pigmentation [ 10 , 11 ]. These peptides can suppress melanin synthesis by targeting the receptors, signaling molecules, and enzymes involved in melanin and melanosome synthesis [ 12 , 13 ].…”

Proteinase-activated Receptor 2: Springboard of Tumors

“…No non-canonical cleavage sites have been described for PAR-3 and -4 and only one for PAR-2 (2). In case of PAR-2, trypsin (not thrombin) cleaves the N-terminal at the R 36 /S 37 cleavage site, revealing the canonical tethered ligand SLIGKV in humans (SLIGRL in mice), while the non-canonical tethered ligand is completely different due to cleavage around serine 67 at sites A 66 /S 67 and S 67 /V 68 , revealing the non-canonical tethered ligand VLTGKL (3). Even though some of these proteases reveal tethered ligands very similar to the canonical ligands, for each of the noncanonical ligands there is also a different signalling outcome through particular PAR.…”