Authors
Ping Li, Xue-Yi Lin, Yu Lin, Yan Liu, Wei-Bing Yang
Published in
Cytotechnology. Volume 78. Issue 5. Pages 172. Epub Aug 08, 2026.
Abstract
SOX4 participates in cell differentiation, but its regulatory function and underlying mechanism in the osteogenic differentiation of MC3T3-E1 cells remain elusive. Immunofluorescence staining was used to detect SOX4 subcellular localization and co-localization with NLRP3. Alizarin Red staining was applied to evaluate osteogenic differentiation. RT-PCR and Western blot assays quantified mRNA and protein levels of SOX4, osteogenic markers (OPN, OCN, RUNX2), inflammatory cytokines, and pyroptosis-related proteins (NLRP3, caspase-1, GSDMD). JASPAR predicted SOX4 binding sites in the NLRP3 promoter and ChIP-qPCR was used to validate it. Dual-luciferase reporter assay was applied to assesse transcriptional regulation. Rescue experiments were performed via co-transfection of SOX4 and NLRP3 overexpression vectors. SOX4 was upregulated during MC3T3-E1 osteogenic differentiation. SOX4 overexpression reduced pro-inflammatory cytokines (TNF-α, IL-1β, IL-6), increased IL-10, and inhibited pyroptosis. SOX4 directly bound to the NLRP3 promoter to suppress its transcription. NLRP3 overexpression reversed SOX4-induced enhancement of osteogenic differentiation and marker expression. SOX4 promotes MC3T3-E1 osteogenic differentiation by directly inhibiting NLRP3 transcription, thereby regulating inflammation and pyroptosis.
The online version contains supplementary material available at 10.1007/s10616-026-01040-5.
PMID:
42572509
Bibliographic data and abstract were imported from PubMed on 10 Aug 2026.
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