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To corroborate these findings on a functional level, we isolated activated ILC2s from IL-33 challenged BALB/c mice ( Figure 3A ), which were then incubated for 24h with either an MT1 agonist (Ramelteon), MT1 antagonist (S-26131), MT2 agonist (Tasimelteon), MT2 antagonist (4-P-PDOT) and/or melatonin ( Figures 3BE )

They added GHK-Cu in concentrations of 10 M to 10 M and measured: Collagen synthesis (by radioactive proline incorporation) Non-collagen protein synthesis Cell proliferation What they found: Stimulation of collagen synthesis by 70 % at the optimal concentration of 10 M (1 nM) The effect was NOT dependent on increased proliferation, fibroblasts increased production per cell Background: GHK without copper had a dramatically weaker effect , Cu is critical Reversibility: After removing GHK-Cu, synthesis returned to baseline Why it matters: This is the fundamental mechanistic study that documented the effect of GHK-Cu on collagen

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The phenotypic switch from M1 to reparative macrophages (M2) is critical for tissue regeneration (Finley et al., 2016