1. Immunology/Inflammation
  2. Osteopontin
  3. SVVYGLR

SVVYGLR 是一种骨桥蛋白衍生肽。SVVYGLR 能够促进成纤维细胞分化为肌成纤维细胞样细胞,并促进心肌成纤维细胞产生 III 型胶原蛋白。SVVYGLR 可在体外激活内皮细胞的黏附、迁移及管形成。SVVYGLR 促进血管形成和伤口愈合,并促进真皮成纤维细胞和角质形成细胞的迁移。SVVYGLR 可用于血管生成、真皮伤口和骨再生相关研究。

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Custom Peptide Synthesis

SVVYGLR

SVVYGLR Chemical Structure

CAS No. : 292851-89-9

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

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[1][2][3].

体外研究
(In Vitro)

SVVYGLR (0.02 μg/mL) 可在体外激活内皮细胞的黏附、迁移和成管作用[1]
SVVYGLR (0.01-100 μg/mL;包被 2 小时,细胞孵育 30 分钟) 可呈浓度依赖性增强 hMSCs、hPLFs、hGFs 和 HUVECs 的黏附能力,在 100 μg/mL 时作用最强[2]
SVVYGLR (1-1000 ng/mL;每 2 天更换培养基持续培养,于第 6 天检测) 可呈浓度依赖性促进 hMSCs、HUVECs 和 hPLFs 的增殖 (对 hGFs 无此作用),在第 6 天 100 ng/mL 浓度下效果最强[2]
SVVYGLR (10-1000 ng/mL;RAW264.7 细胞处理 5 天,BMMs 处理 10 天) 可抑制 RAW264.7 细胞和 BMMs 中的破骨细胞生成,在 100 ng/mL 浓度下抑制作用显著[2]
SVVYGLR (100 ng/mL;作用 24、72、96 h) 可在 100 ng/mL 浓度下抑制 RANKL 诱导的 pNFAT/Luc-RAW264.7 细胞中 NFAT 的活性[2]
SVVYGLR (100 ng/mL;作用 3、5 天) 可在 RANKL 刺激的 RAW264.7 细胞中以 100 ng/mL 的浓度下调破骨细胞生成标记基因 (降钙素受体、组织蛋白酶 K、TRAP) 及整合素 α9 的表达[2]
SVVYGLR (10 ng/mL;36 h) 可在 36 h 时显著促进大鼠真皮成纤维细胞 (RDFs) 向划痕创面区域迁移[3]
SVVYGLR (10 ng/mL; 10 h) 可在 10 小时时显著促进人表皮角质形成细胞 (HEKa) 向划痕损伤区域迁移[3]
SVVYGLR (10 ng/mL;3 h) 在 3 小时的趋化小室迁移实验中显著增强大鼠真皮成纤维细胞 (RDFs) 和人上皮角质形成细胞 (HEKa) 的迁移活性[3]

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Proliferation Assay[2]

Cell Line: hMSCs, hPLFs, hGFs, HUVECs
Concentration: 1-1000 ng/mL
Incubation Time: 6 days
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.

RT-PCR[2]

Cell Line: RAW264.7 cells
Concentration: 100 ng/mL
Incubation Time: 3, 5 days
Result: Decreased mRNA expression of calcitonin receptor, cathepsin K, TRAP, and integrin α9 in RANKL-stimulated cells relative to RANKL-only controls.

Cell Migration Assay[3]

Cell Line: Rat dermal fibroblasts (RDFs)
Concentration: 10 ng/mL
Incubation Time: 0, 12, 24, 36 h
Result: Significantly accelerated migration into the scratch wound area at 36 h compared with untreated controls and scrambled SV peptide (rSV)-treated groups.

Cell Migration Assay[3]

Cell Line: Human epithelial keratinocytes (HEKa)
Concentration: 10 ng/mL
Incubation Time: 0, 5, 10 h
Result: Significantly accelerated migration into the scratch wound area at 10 h compared with untreated controls and rSV-treated groups.

Cell Migration Assay[3]

Cell Line: Rat dermal fibroblasts (RDFs) and Human epithelial keratinocytes (HEKa)
Concentration: 10 ng/mL
Incubation Time: 3 h
Result: Significantly enhanced migratory activity compared with untreated controls and rSV-treated groups.

Cell Proliferation Assay[3]

Cell Line: Rat dermal fibroblasts (RDFs) and human epithelial keratinocytes (HEKa)
Concentration: 10 ng/mL
Incubation Time: 24, 48, 72, 96 h
Result: Showed no significant differences in proliferation compared with rSV-treated and untreated controls over 24-96 h.
体内研究
(In Vivo)

SVVYGLR (0.02 µg/mL;通过扩散室植入;持续 5 天) 在背部气囊模型中可显著诱导小鼠体内血管生成,平均血管生成分级为 2.00[1]
SVVYGLR (10 µg;通过胶原海绵植入;缺损创建时单次给药) 可在大鼠颅骨缺损模型中于 3 周时抑制骨缺损部位的破骨细胞数量,并在 5 周时促进胶原海绵吸收及致密骨形成[2]
SVVYGLR (12.5 μg/gel;以 Medgel 载体经局部给药;伤口形成时单次给药) 在大鼠中通过刺激成纤维细胞迁移、成纤维细胞向肌成纤维细胞分化及血管生成来促进皮肤伤口愈合[3]

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: BALB/cAnNCrj (6-week-old female)[1]
Dosage: 0.02 µg/mL
Administration: Implanted via diffusion chamber; 5 days
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).
Animal Model: Sprague-Dawley (male, 12-week-old, artificial bone defect model)[2]
Dosage: 10 µg
Administration: implanted via collagen sponge; single administration at the time of defect creation
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。
Animal Model: Sprague-Dawley (male, 8-week-old, full-thickness 5-mm skin wound model)[3]
Dosage: 12.5 μg/gel
Administration: topical via Medgel; single application at wound creation
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.
分子量

792.92

Formula

C36H60N10O10

CAS 号
Sequence

Ser-Val-Val-Tyr-Gly-Leu-Arg

Sequence Shortening

SVVYGLR

运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.

纯度 & 产品资料
参考文献
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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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SVVYGLR
目录号:
HY-P11648
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