SVVYGLR

SVVYGLR is a peptide derived from osteopontin. It facilitates the differentiation of fibroblasts into myofibroblast-like cells and enhances the production of type III collagen by cardiac fibroblasts. In vitro, SVVYGLR activates endothelial cell adhesion, migration, and tube formation. Additionally, it promotes angiogenesis, wound healing, and the migration of dermal fibroblasts and keratinocytes. SVVYGLR is applicable in studies related to angiogenesis, dermal wounds, and bone regeneration.

SVVYGLR, at a concentration of 0.02 μg/mL, can activate endothelial cell adhesion, migration, and tube formation in vitro. When used at 0.01-100 μg/mL (coated for 2 hours, cell incubation for 30 minutes), it enhances the adhesion capability of hMSCs, hPLFs, hGFs, and HUVECs in a concentration-dependent manner, with the strongest effect at 100 μg/mL. At 1-1000 ng/mL (media changed every two days with detection on the 6th day), SVVYGLR promotes the proliferation of hMSCs, HUVECs, and hPLFs dose-dependently, without affecting hGFs, showing the strongest effect at 100 ng/mL on day six. Furthermore, when applied at 10-1000 ng/mL (5 days for RAW264.7 cells, 10 days for BMMs), it inhibits osteoclastogenesis in RAW264.7 cells and BMMs, with significant suppression at 100 ng/mL. At 100 ng/mL (24, 72, 96 h duration), SVVYGLR suppresses NFAT activity in pNFAT/Luc- RAW264.7 cells induced by RANKL. It also downregulates expression of osteoclastogenesis marker genes (calcitonin receptor, cathepsin K, TRAP) and integrin α9 in RANKL-stimulated RAW264.7 cells at a 100 ng/mL concentration over 3-5 days. In migration studies, SVVYGLR at 10 ng/mL significantly enhances the migration of rat dermal fibroblasts (RDFs) to scratch wound areas within 36 hours, while similarly promoting human epidermal keratinocyte (HEKa) migration to damaged regions in 10 hours, and increasing migration activity of RDFs and HEKa in a 3-hour chemotaxis chamber assay.

SVVYGLR (0.02 µg/mL; implanted via diffusion chamber; duration of 5 days) significantly induces angiogenesis in the dorsal air pouch model in mice, with an average angiogenesis score of 2.00. In a rat cranial defect model, SVVYGLR (10 µg; single administration via collagen sponge at defect creation) suppresses osteoclast numbers at the defect site at 3 weeks and promotes collagen sponge absorption and compact bone formation at 5 weeks. Moreover, in rats, SVVYGLR (12.5 μg/gel; administered locally using Medgel carrier; single administration at wound creation) enhances skin wound healing by stimulating fibroblast migration, fibroblast differentiation into myofibroblasts, and angiogenesis.