Protocol tests resolvin-induced TGF-β1 secretion

This proposed study asks whether ageing macrophages, immune cells that shape stem-cell support, release more scar-promoting protein after an inflammation-resolving signal. Resolvin D1 would be tested in human macrophages with sparse FPR2, a surface receptor. Researchers would measure transforming growth factor beta-1, a protein linked to fibrosis, in untreated cells and cells given resolvin D1, beta-arrestin-2 small interfering RNA, a gene-silencing tool, or pertussis toxin, which disrupts G-alpha-i signaling. A rise blocked by the RNA but retained with toxin would support the proposed receptor switch. Low FPR2 must first be verified by flow cytometry, a cell-surface measurement.