ArticleJournal of molecular cell biology2026
Sublytic C5b-9 induces S100A8/A9 expression via SMYD4-dependent SOX7-K159 methylation in the glomerular mesangial cells of Thy-1 nephritis rats.
Article in Journal of molecular cell biology, 2026. 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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Abstract
Rat Thy-1 nephritis (Thy-1N) is a model for human mesangioproliferative glomerulonephritis (MsPGN). Although sublytic C5b-9 has been reported to affect pro-inflammatory cytokine expression in glomerular mesangial cells (GMCs), the induction of other pro-inflammatory mediators remains unclear. In this study, we demonstrated that SET and MYND domain-containing protein 4 (SMYD4), SRY-related HMG-box gene 7 (SOX7), S100 calcium-binding protein A8 (S100A8), and S100A9 were overexpressed in the renal tissues of Thy-1N rats and in the GMCs stimulated by sublytic C5b-9. Mechanistically, SOX7 triggered S100A8/A9 gene transcription through binding to S100A8 promoter (+21 to +31 nt) and S100A9 promoter (-1698 to -1688 nt), and SMYD4 mediated SOX7 methylation at K159, a new methylation site, enhancing SOX7 function and S100A8/A9 transcription. The animal experiments confirmed that silencing SMYD4, SOX7, or S100A8/A9 gene could inhibit GMC proliferation, extracellular matrix accumulation, and proteinuria in Thy-1N rats. Moreover, silencing SMYD4 gene could inhibit renal SOX7-K159me2/3, and silencing SMYD4 or SOX7 gene could inhibit renal S100A8/A9 production. Meanwhile, the SOX7-K159 methylation inhibitory peptide exhibited the similar intervention effects as SMYD4 and SOX7 knockdown in Thy-1N rats. In addition, the expression levels of SMYD4, SOX7, SOX7-K159me2/3, and S100A8/A9 all increased in the renal tissues of MsPGN patients. Collectively, our findings suggest that SMYD4-mediated SOX7-K159me2/3 partly contributes to sublytic C5b-9-induced S100A8/A9 expression in Thy-1N rats, which provides a novel insight into human MsPGN pathogenesis.
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