Dataset Information

17β-Estradiol promotes angiogenesis of bone marrow mesenchymal stem cells by upregulating the PI3K-Akt signaling pathway

ABSTRACT: Graphical abstract Highlights • The role and mechanism of 17β -estradiol in the regulation of BMSC promoting angiogenesis were analyzed by bioinformatics techniques for the first time.• Combined with FN1, MCM2, XPO1, NTRK1 and other proteins, 17β-estradiol is able to activate PI3K-Akt, MAPK and other signaling pathways to regulate BMSCs to promote or remodel angiogenesis.• 17β-estradiol upregulates the PI3K-Akt signaling pathway to promote the BMSC angiogenesis process of differentiation.

Objective

Estrogen is an important hormone affecting angiogenesis in women and is important for female physical development. Menopausal women are prone to serious cardiovascular and cerebrovascular diseases when estrogen is significantly reduced. Bone marrow mesenchymal stem cells (BMSC) have potential roles in processes such as angiogenesis and remodeling. This study is to investigate the effect of 17β-estradiol on BMSC angiogenic differentiation and its underlying molecular mechanism, and to provide a basis for the treatment of microvascular diseases.

Methods

Enrichment analysis of apoptosis, migration or angiogenesis processes and molecular mechanisms of BMSC treated with 17β-estradiol was performed to screen core proteins and perform molecular docking validation. Human MSCs were cultured in vitro to examine the effect of 17β-estradiol on BMSC migration or angiogenic differentiation.

Results

17β-estradiol acted on 48 targets of BMSC and was involved in regulating 52 cell migration processes or 17 angiogenesis processes through 66 KEGG pathways such as PI3K-Akt, MAPK, etc. 17β-estradiol bound tightly to 10 core proteins including APP, NTRK1, EGFR, and HSP90AA1. 17β-estradiol promoted cell scratch area closure rate and CD31 expression in BMSCs, downregulated BMSC apoptosis rate, and promoted Akt and p-Akt protein expression in BMSC.

Conclusion

17β-estradiol binds to FN1, MCM2, XPO1, NTRK1 and other proteins to initiate PI3K-Akt, MAPK and other signaling pathways, so as to regulate BMSC to promote or remodel angiogenesis, verifying that 17β-estradiol up-regulates PI3K-Akt signaling pathway to promote BMSC angiogenic differentiation.

SUBMITTER: Zhang X

PROVIDER: S-EPMC9309573 | biostudies-literature |

REPOSITORIES: biostudies-literature

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