Prof. Kun Xiao | Publications & Academic Profile | SinoBioData

Research Publications & English Decoded Briefs

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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•2026•DOI: 10.3724/abbs.2026066

FGF10 is essential for postnatal meibomian gland development in mice

Fibroblast growth factor 10 (FGF10) plays a critical role in ocular surface homeostasis, yet its function in early meibomian gland (MG) development remains largely unknown. Here, we generated an Fgf10 mutant mouse model with deletion of exon 2, leading to loss of function. Adult Fgf10+/− mice exhibited lacrimal gland agenesis, smaller Harderian glands, increased corneal fluorescein staining, and reduced tear volume. Histological analysis revealed multilayered hyperplastic epithelium in Harderian glands and MG atrophy. Time-series Oil Red O staining showed shorter, thinner, and disordered MGs in Fgf10+/− mice at P14 and P21, with unrecoverable defects at P135. RNA sequencing of MGs at P14 and P21 revealed significant dysregulation of macrophage-related genes and immune-related pathways, including antigen processing and presentation and macrophage chemotaxis. Using Cx3cr1GFP/+ reporter mice, we observed a significant reduction in CX3CR1-positive cells in the inter-acinar stroma of Fgf10+/− MGs. Pharmacological ablation of CSF1R-expressing cells with PLX3397 in wild-type mice recapitulated the MG developmental defects, confirming that FGF10 acts through immune cells to regulate MG development. Collectively, our findings establish that FGF10 haploinsufficiency leads to severe glandular malformations, impaired tear production, and compromised corneal integrity, highlighting the essential role of FGF10 in postnatal MG development and immune cell regulation.

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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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