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SIKVAV促进血管内皮细胞的增殖和相关机制
Xionglin Chen1, Jie Zhang1, Xiaoming Cao2
1Department of Histology, Embryology and Medical Genetics, Jiangxi Provincial Key Laboratory of Cell Precision Therapy, School of Basic Medical Sciences, Jiujiang University, Jiujiang, China.
Bio-medical materials and engineering
|September 6, 2024
概括
SIKVAV通过激活关键信号通路,显著增强血管内皮细胞的增殖和迁移. 这种可以通过组织工程治疗皮肤伤口和缺血性疾病.
科学领域:
- 生物材料科学 生物材料科学
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 糖尿病足 (DFU) 涉及血管内皮损伤,损害细胞增殖和迁移.
- 低氧诱导因子,生长因子和炎症调节DFU中的内皮细胞功能.
研究的目的:
- 评估SIKVAV (Ser-Ile-Lys-Val-Ala-Val) 对小鼠大动脉内皮细胞 (MAEC) 增殖和迁移的影响.
- 阐明SIKVAV对MAEC的作用背后的分子机制.
主要方法:
- 随着时间的推移 (0-72小时),MAEC患者接受了不同度的SIKVAV (0-600微克/毫升) 治疗.
- 使用CCK-8试验评估了细胞活力.
- 增殖标记PCNA和信号蛋白ERK1/2和Akt的表达通过qRT-PCR和西部斑块测量.
主要成果:
- 根据SIKVAV的剂量增加了PCNA mRNA和MAEC的扩散.
- SIKVAV上调酸化ERK1/2 (p-ERK1/2) 和Akt (p-Akt),是MAPK/ERK1/2和PI3K/Akt通路的关键组成部分.
- 抑制这些途径降低了PCNA表达,增殖和p-ERK1/2/p-Akt水平,证实了SIKVAV的机制.
结论:
- SIKVAV加速了血管内皮细胞的增殖,这表明它在皮肤伤口治疗中有用,当它被移植到支架上时.
- 这些发现为在缺血性疾病的组织工程中使用SIKVAV提供了理论基础.
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