ArticleCell death discovery2025
KDM4B modulates ERα signaling pathway to participate in vascular smooth muscle cell calcification.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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17 authors.
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Abstract
Vascular calcification (VC) is recognized as an independent predictor of cardiovascular events. Although estrogen replacement is a controversial treatment due to its potential carcinogenic effects, it was considered a protective treatment against VC in postmenopausal women. Estrogen receptor α (ERα) co-regulators were considered as potential therapeutic targets for ERα-related cancers. However, ERα activity and the biological function modulation of ERα co-regulators in VC remain elusive. Histone lysine demethylase 4B (KDM4B) was identified to be highly expressed in human and mouse aortic smooth muscle (ASMC) cells treated with β-phosphoglycerol and in mice overloaded with VitD3 during calcification, as evidenced by western blotting and immunofluorescence staining. Co-immunoprecipitation (Co-IP) was performed to show the association between KDM4B and ERα. Our data demonstrated that KDM4B down-regulated ERα-induced transactivation and that KDM4B depletion increased mRNA expression of endogenous ERα target genes. Furthermore, we provided the evidence to show that KDM4B is associated with Polycomb repressive complex 2 (PRC2) and ERα. In addition, KDM4B depletion decreased the recruitment of PRC2 complex to estrogen response element (ERE) regions of ERα target gene, thereby down-regulating the H3K27me3 levels. Finally, KDM4B-mediated enhancement of ASMCs' calcification was partially attenuated by the estrogen treatment. KDM4B inhibits ERα-induced transactivation independent of its Jumanji-C enzyme active region. Taken together, our study suggests that KDM4B acting as ERα co-repressor is involved in the regulation of VC, indicating that KDM4B may be a new potential therapeutic target for VC treatment.
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