COMMD10通过Rap1信号通路调控血管生成和骨形成

IF 2.5 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Peiran Li, Yanxi Li
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引用次数: 0

摘要

铜代谢MURR1结构域蛋白10 (COMMD10)调节许多对细胞稳态至关重要的生物过程。然而,COMMD10在血管生成和骨形成中的作用仍未被探索。我们在内皮细胞中构建COMMD10敲低模型,并测定COMMD10对血管生成和骨形成的影响。我们的研究结果表明,COMMD10敲低通过影响内皮细胞中与血管生成相关的基因和蛋白质的表达来促进血管形成。此外,表达低水平COMMD10的内皮细胞通过分泌促成骨因子促进骨形成。此外,Rap1信号通路在低COMMD10条件下被激活。RAP1B和COMMD10的双敲低降低了内皮细胞的血管生成能力。综上所述,我们的研究表明,低COMMD10表达通过Rap1信号通路促进血管生成和骨形成。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
COMMD10 Regulates Angiogenesis and Bone Formation via Rap1 Signaling Pathway

Copper metabolism MURR1 domain protein 10 (COMMD10) regulates numerous biological processes that are essential for cellular homeostasis. However, the role of COMMD10 in angiogenesis and bone formation remains unexplored. We constructed a COMMD10 knockdown model in endothelial cells and determined the influence of COMMD10 on angiogenesis and bone formation. Our results indicate that COMMD10 knockdown enhances vascular formation by influencing the expression of genes and proteins related to angiogenesis in endothelial cells. In addition, endothelial cells expressing low levels of COMMD10 facilitate bone formation by secreting pro-osteogenic factors. Further, the Rap1 signaling pathway is activated under low COMMD10 conditions. Double knockdown of RAP1B and COMMD10 attenuated the angiogenic ability of endothelial cells. In summary, our research demonstrates that low COMMD10 expression promotes angiogenesis and bone formation through the Rap1 signaling pathway.

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来源期刊
FASEB bioAdvances
FASEB bioAdvances Multiple-
CiteScore
5.40
自引率
3.70%
发文量
56
审稿时长
10 weeks
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