SVVYGLR
SVVYGLR is an osteopontin-derived peptide. SVVYGLR can promote the differentiation of fibroblasts into myofibroblast-like cells and promote the production of type III collagen by cardiac fibroblasts. SVVYGLR can activate the adhesion, migration and tubule formation of endothelial cells in vitro. SVVYGLR promotes angiogenesis and wound healing and promotes the migration of dermal fibroblasts and keratinocytes. SVVYGLR can be used for research related to angiogenesis, dermal wounds and bone regeneration.
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- CAS No.: 292851-89-9
- 화학식: C36H60N10O10
- 분자량:792.92
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- 순도&문서
- References
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Help & FAQs
Biological Activity
SVVYGLR (0.02 μg/mL) activates adhesion, migration, and tube formation by endothelial cells in vitro[1].
SVVYGLR (0.01-100 μg/mL; 2 h coating, 30 min cell incubation) enhances adhesion of hMSCs, hPLFs, hGFs, and HUVECs in a concentration-dependent manner, with the strongest effect at 100 μg/mL[2].
SVVYGLR (1-1000 ng/mL; continuous culture with medium renewal every other day, measured on day 6) enhances proliferation of hMSCs, HUVECs, and hPLFs (but not hGFs) in a concentration-dependent manner, with the strongest effect at 100 ng/mL on day 6[2].
SVVYGLR (10-1000 ng/mL; 5 days for RAW264.7 cells, 10 days for BMMs) suppresses osteoclastogenesis in RAW264.7 cells and BMMs, with significant inhibition at 100 ng/mL[2].
SVVYGLR (100 ng/mL; 24, 72, 96 h) suppresses RANKL-induced NFAT activity in pNFAT/Luc-RAW264.7 cells at 100 ng/mL[2].
SVVYGLR (100 ng/mL; 3, 5 days) downregulates expression of osteoclastogenic marker genes (calcitonin receptor, cathepsin K, TRAP) and integrin α9 in RANKL-stimulated RAW264.7 cells at 100 ng/mL[2].
SVVYGLR (10 ng/mL; 36 h) significantly accelerates the migration of rat dermal fibroblasts (RDFs) into scratch wound areas at 36 h[3].
SVVYGLR (10 ng/mL; 10 h) significantly accelerates the migration of human epithelial keratinocytes (HEKa) into scratch wound areas at 10 h[3].
SVVYGLR (10 ng/mL; 3 h) significantly enhances the migratory activity of rat dermal fibroblasts (RDFs) and human epithelial keratinocytes (HEKa) in a 3-hour Chemotaxicell migration assay[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:hMSCs, hPLFs, hGFs, HUVECs
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Concentration:1-1000 ng/mL
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Incubation Time:6 days
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Result:Enhanced proliferation of hMSCs 1.4-fold, HUVECs 1.2-fold, and hPLFs 1.1-fold at 100 ng/ml on day 6 in a concentration-dependent manner. Did not affect hGF proliferation.
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Cell Line:RAW264.7 cells
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Concentration:100 ng/mL
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Incubation Time:3, 5 days
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Result:Decreased mRNA expression of calcitonin receptor, cathepsin K, TRAP, and integrin α9 in RANKL-stimulated cells relative to RANKL-only controls.
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Cell Line:Rat dermal fibroblasts (RDFs)
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Concentration:10 ng/mL
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Incubation Time:0, 12, 24, 36 h
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Result:Significantly accelerated migration into the scratch wound area at 36 h compared with untreated controls and scrambled SV peptide (rSV)-treated groups.
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Cell Line:Human epithelial keratinocytes (HEKa)
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Concentration:10 ng/mL
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Incubation Time:0, 5, 10 h
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Result:Significantly accelerated migration into the scratch wound area at 10 h compared with untreated controls and rSV-treated groups.
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Cell Line:Rat dermal fibroblasts (RDFs) and Human epithelial keratinocytes (HEKa)
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Concentration:10 ng/mL
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Incubation Time:3 h
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Result:Significantly enhanced migratory activity compared with untreated controls and rSV-treated groups.
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Cell Line:Rat dermal fibroblasts (RDFs) and human epithelial keratinocytes (HEKa)
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Concentration:10 ng/mL
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Incubation Time:24, 48, 72, 96 h
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Result:Showed no significant differences in proliferation compared with rSV-treated and untreated controls over 24-96 h.
SVVYGLR (10 µg; implanted via collagen sponge; single administration at the time of defect creation) suppresses osteoclast numbers in bone defects at 3 weeks and enhances collagen sponge resorption and compact bone formation by 5 weeks in a rat calvarial defect model[2].
SVVYGLR (12.5 μg/gel; topical via Medgel; single application at wound creation) promotes dermal wound healing by stimulating fibroblast migration, myofibroblastic differentiation of fibroblasts, and angiogenesis in rats[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/cAnNCrj (6-week-old female)[1]
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Dosage:0.02 µg/mL
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Administration:Implanted via diffusion chamber; 5 days
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Result:Achieved a mean angiogenesis grade of 2.00; induced spiral and immature blood vessels; reached an angiogenic level approximately the same as that of vascular endothelial growth factor (VEGF).
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Animal Model:Sprague-Dawley (male, 12-week-old, artificial bone defect model)[2]
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Dosage:10 µg
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Administration:implanted via collagen sponge; single administration at the time of defect creation
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Result:Reduced number of TRAP-positive osteoclasts in bone defect area significantly compared to controls at 3 weeks post-operation; Decreased area of remaining collagen sponge significantly compared to controls at 5 weeks post-operation; Induced new bone formation extending to the periosteal surface (with compact bone morphology and cement lines) surrounding the sponge graft at 5 weeks post-operation。
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Animal Model:Sprague-Dawley (male, 8-week-old, full-thickness 5-mm skin wound model)[3]
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Dosage:12.5 μg/gel
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Administration:topical via Medgel; single application at wound creation
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Result:Accelerated wound closure compared to control and PBS groups (significant at days 6 and 8); Increased migration of HSP-47-positive fibroblasts to the wound area at day 4; Significantly enhanced number of α-SMA-positive myofibroblasts in the wound area at day 14; Marked increase in von Willebrand factor-positive neomicrovessels at day 7.
Chemical Information
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CAS No. 292851-89-9
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분자량 792.92
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화학식 C36H60N10O10
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Sequence
Ser-Val-Val-Tyr-Gly-Leu-Arg
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Sequence Shortening
SVVYGLR
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
순도&문서
References
[1]. Hamada Y, et al. Osteopontin-derived peptide SVVYGLR induces angiogenesis in vivo. Dent Mater J. 2004;23(4):650-655. [Content Brief]
[2]. Egusa H, et al. Enhanced bone regeneration via multimodal actions of synthetic peptide SVVYGLR on osteoprogenitors and osteoclasts. Biomaterials. 2009;30(27):4676-4686. [Content Brief]
[3]. Uchinaka A, et al. Evaluation of dermal wound healing activity of synthetic peptide SVVYGLR. Biochem Biophys Res Commun. 2017;491(3):714-720. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
SVVYGLR Related Classifications
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