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COMMD10通过Rap1信号通路调节血管生成和骨形成。

COMMD10 Regulates Angiogenesis and Bone Formation via Rap1 Signaling Pathway.

作者信息

Li Peiran, Li Yanxi

机构信息

Department of Plastic and Traumatic Surgery School of Stomatology, Beijing Stomatological Hospital, Capital Medical University Beijing China.

Department of Dental Implant Center School of Stomatology, Beijing Stomatological Hospital, Capital Medical University Beijing China.

出版信息

FASEB Bioadv. 2025 May 26;7(6):e70016. doi: 10.1096/fba.2024-00159. eCollection 2025 Jun.

DOI:10.1096/fba.2024-00159
PMID:40496352
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12147500/
Abstract

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.

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学过程。然而，COMMD10在血管生成和骨形成中的作用仍未得到探索。我们构建了内皮细胞中COMMD10基因敲低模型，并确定了COMMD10对血管生成和骨形成的影响。我们的结果表明，COMMD10基因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表达来增强血管形成。此外，表达低水平COMMD10的内皮细胞通过分泌促骨生成因子促进骨形成。此外，在COMMD10水平较低的条件下，Rap1信号通路被激活。RAP1B和COMMD10的双重敲低减弱了内皮细胞的血管生成能力。总之，我们的研究表明，低水平的COMMD10表达通过Rap1信号通路促进血管生成和骨形成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d5/12147500/b98115749268/FBA2-7-e70016-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d5/12147500/bcdb1d4b7a4d/FBA2-7-e70016-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d5/12147500/354ae2c4752a/FBA2-7-e70016-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d5/12147500/bf8672ca14fa/FBA2-7-e70016-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d5/12147500/bc96f62b60d2/FBA2-7-e70016-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d5/12147500/1a808fbc83d9/FBA2-7-e70016-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d5/12147500/b98115749268/FBA2-7-e70016-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d5/12147500/bcdb1d4b7a4d/FBA2-7-e70016-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d5/12147500/354ae2c4752a/FBA2-7-e70016-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d5/12147500/bf8672ca14fa/FBA2-7-e70016-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d5/12147500/bc96f62b60d2/FBA2-7-e70016-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d5/12147500/1a808fbc83d9/FBA2-7-e70016-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0d5/12147500/b98115749268/FBA2-7-e70016-g005.jpg

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