Prof. Yue’e Chai | Publications & Academic Profile | SinoBioData

Research Publications & English Decoded Briefs

Showing 3 publications

Acta Biochimica et Biophysica Sinica•2024•DOI: 10.3724/abbs.2024024

The mechanism by which piR-000699 targets SLC39A14 regulates ferroptosis in aging myocardial ischemia/reperfusion injury

Myocardial ischemia/reperfusion (I/R) injury is a classic type of cardiovascular disease characterized by injury to cardiomyocytes leading to different types of cell death. The degree of irreversible myocardial damage is closely related to age, and ferroptosis is involved in cardiomyocyte damage. However, the mechanisms underlying ferroptosis regulation in aging myocardial I/R injury are still unclear. The present study aims to explore the underlying mechanism of piRNA regulation in ferroptosis. Using left anterior descending coronary artery ligation in an aging rat model and a D-galactose-induced rat cardiomyocyte line (H9C2) to construct an aging cardiomyocyte model, we investigate whether ferroptosis occurs after reperfusion injury in vitro and in vivo. This study focuses on the upregulation of piR-000699 after hypoxia/reoxygenation treatment in aging cardiomyocytes by observing hypoxia/reoxygenation (H/R) injury indicators and ferroptosis-related indicators and clarifying the role of piR-000699 in H/R injury caused by ferroptosis in aging cardiomyocytes. Bioinformatics analysis reveals that SLC39A14 is a gene that binds to piR-000699. Our data show that ferroptosis plays an important role in I/R injury both in vivo and in vitro. Furthermore, the results show the potential role of piR-000699 in regulating SLC39A14 in ferroptosis in aging cardiomyocytes under hypoxia/reoxygenation conditions. Together, our results reveal that the mechanism by which piR-000699 binds to SLC39A14 regulates ferroptosis in aging myocardial I/R injury.

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Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025096

Dexamethasone induces ferroptosis in MC3T3-E1 cells by promoting DNMT3a-mediated Sirt1 DNA hypermethylation in the context of steroid-induced osteonecrosis of the femoral head

Ferroptosis, a novel form of regulated necrosis, has drawn the attention of the scientific community. Nevertheless, few studies have focused on the impact of ferroptosis on MC3T3-E1 cells in the context of steroid-induced osteonecrosis of the femoral head (SONFH). In this study, we explore the relationship between the degree of ferroptosis induced by dexamethasone (Dex) and the expression of silent information regulatory protein 1 (Sirt1). The results indicate that the ferroptosis level induced by Dex is mediated by the downregulation of Sirt1. Overexpression of Sirt1 increases the levels of the ferroptosis-related proteins SLC7A11 and GPX4 in MC3T3-E1 cells following Dex exposure. Moreover, the effect of Dex on Sirt1 expression is regulated by hypermethylation of the Sirt1 promoter, which is catalyzed by DNA methyltransferase 3a (DNMT3a). In summary, this study reveals that Dex can trigger ferroptosis by promoting DNMT3a-mediated DNA methylation and downregulating Sirt1 expression. Our findings provide an additional new mechanism for Dex-induced ferroptosis in MC3T3-E1 cells.

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Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025096

Dexamethasone Induces Ferroptosis in MC3T3-E1 Cells by Promoting DNMT3a-Mediated Sirt1 DNA Hypermethylation in the Context of Steroid-Induced Osteonecrosis of the Femoral Head

Steroid-induced osteonecrosis of the femoral head (SONFH) is a progressive bone disorder driven by prolonged glucocorticoid exposure, with limited therapeutic options. Ferroptosis, a regulated form of necrosis, has emerged as a potential contributor to SONFH pathogenesis, yet its mechanistic link to osteoblast dysfunction remains poorly defined. This study investigates the relationship between dexamethasone (Dex)-induced ferroptosis and silent information regulator 1 (Sirt1) in MC3T3-E1 osteoblastic cells. Dex treatment downregulated Sirt1 expression and increased ferroptosis markers, while Sirt1 overexpression elevated the ferroptosis-related proteins SLC7A11 and GPX4 following Dex exposure. Mechanistically, Dex promoted hypermethylation of the Sirt1 promoter via DNA methyltransferase 3a (DNMT3a), leading to Sirt1 suppression. These findings establish a novel epigenetic axis—DNMT3a-mediated Sirt1 promoter hypermethylation—that drives Dex-induced ferroptosis in osteoblasts. The study was conducted exclusively in vitro, and the pathophysiological relevance requires validation in animal models. Nevertheless, this work provides a foundation for understanding the epigenetic regulation of osteoblast ferroptosis and suggests potential therapeutic avenues for preventing SONFH.

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