ArticleBiological trace element research2026
Selenoprotein S Deficiency Induces Matrix Degradation Via TGF-β Pathway Leading to Cartilage Damage.
Article in Biological trace element research, 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
The deficiency of trace element selenium is a global nutritional issue. Selenium exerts its biological functions in the human body through selenoproteins, which play crucial roles in bone and cartilage development. Selenoprotein S (SelS), a key selenoprotein involved in the regulation of oxidative stress and inflammation, has not been fully elucidated in cartilage development. The purpose of this study was to investigate the effects of SelS deficiency on cartilage matrix degradation. Chondrocytes with SelS gene knockdown (sh-Sels) and mice with SelS gene knockout were constructed. The mRNA and protein levels of type II collagen (COL II), matrix metalloproteinases (MMP3, MMP10 and MMP13) were measured by RT-qPCR and western blotting, respectively. Changes in cartilage morphology and matrix composition were evaluated using histological staining techniques, including toluidine blue (TB), safranin O-fast green, and sirius red staining. The expression levels of MMP3, MMP13, MMP19 and COL II in the knee joints of mice were detected by immunohistochemical (IHC) staining. A TGF-β pathway inhibitor (GW788388) was administered to SelS knockdown chondrocytes to verify whether the TGF-β signaling pathway was involved in the matrix degradation induced by SelS deficiency. Compared with the negative vector control (sh-NC) group, the mRNA and protein levels of COL II were decreased in the sh-Sels group. The expression levels of Mmp3, Mmp10 and Mmp13 were also increased significantly, while the metallopeptidase inhibitor Timp2 was downregulated in the sh-Sels group. SelS gene knockout in mice did not affect body length or weight but resulted in reduced proteoglycan and collagen content in articular cartilage. Compared with wild-type mice, the expression of COL II was decreased, while the expressions of MMP3, MMP13, and MMP19 were increased in the articular cartilage of SelS knockout mice. Furthermore, treatment with the TGF-β pathway inhibitor (GW788388) partially rescued the reduction in Col2a1 expression induced by SelS deficiency. SelS plays a crucial role in maintaining cartilage homeostasis, and its deficiency results in cartilage matrix degradation. The TGF-β signaling pathway is involved in the degradation of cartilage matrix caused by SelS silencing. This study provides novel insights into the treatment of fibrotic and degenerative cartilage diseases by focusing on selenoproteins.
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