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Endothelial cell activation sustains estradiol-independent long-term sterile inflammation and promotes endometrial hyperplasia

ABSTRACT: In this study, we elucidate that increased expression of SHP2 in endothelial cells drives the inflammatory activation of endothelial cell through dephosphorylation of its substrate RIPK1 at Y380 site and thus further makes endothelial dysfunction by influencing the transcript factors AP-1 and its target gene IGF1 and inflammatory related genes. The inflammatory activated endothelial cells recruited and activated macrophages, which enhances the inflammatory activation of endothelial cells in a positive feedback manner. Increased growth factor IGF1 in tissue leads to abnormal gland epithelial cell proliferation. Therefore, all the results indicate the importance of tissue endothelial cells and long-term estradiol independent sterile tissue inflammation as regulators of the endometrium hyperplasia. Targeting tissue inflammation through SHP2 inhibition or other anti-inflammation strategies may be potential interventions of EH.

ORGANISM(S): Homo sapiens

PROVIDER: GSE247027 | GEO | 2024/10/31

REPOSITORIES: GEO

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Endothelial Shp2 deficiency controls alternative activation of macrophage preventing radiation-induced lung injury through Notch signaling

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Endothelial cell activation sustains estradiol-independent long-term sterile inflammation and promotes endometrial hyperplasia

Project description:Endothelial cell activation sustains estradiol-independent long-term sterile inflammation and promotes endometrial hyperplasia

| PRJNA1035778 | ENA

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