Tetranectin is significantly elevated in the synovial fluid of patients with full-thickness rotator cuff tears

Figures

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  Fig. 1. (A) Schematic representation of the proteomics workflow used for synovial fluid analysis, including sample preparation, LC-MS/MS acquisition, and data processing. (B) Hierarchical clustering heatmap showing distinct protein expression profiles between the full-thickness tear and control groups. (C) Principal component analysis (PCA) plot illustrating sample distribution based on protein expression variance. (D) Bar graph of the top 10 enriched Gene Ontology Biological Process (GOBP) terms identified from the synovial fluid proteome.

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  Fig. 2. (A) Volcano plot of differentially expressed proteins (DEPs) between groups. Vertical dashed lines indicate the fold-change threshold (|FC| ≥ 1.2), and the horizontal dashed line marks the significance cutoff (p-value < 0.1). (B) Bar chart showing the top five enriched Gene Ontology (GO) terms across Biological Process (GOBP), Molecular Function (GOMF), and Cellular Component (GOCC) categories. Enrichment analysis highlights biological pathways and molecular functions associated with rotator cuff pathology.

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  Fig. 3. (A) Protein-protein interaction (PPI) network of proteins prioritized under exploratory differential-expression criteria between the full-thickness rotator cuff tear group (n = 7) and the partial-thickness tear control group (n = 3). Interactions were retrieved from the STRING database and visualized in Cytoscape. Node color indicates the direction and magnitude of change (log2 fold change; full-thickness vs. control; red, upregulated; blue, downregulated). Node size is proportional to –log10 (nominal p-value), reflecting relative strength of the group difference within the prioritized set. Edges represent known or predicted protein-protein associations. (B) Log2-transformed LFQ intensities (LOD-based imputation for visualization/sensitivity analysis) are shown as mean ± SD with individual values; Welch’s t-test was used (* p < 0.05). BH-adjusted q-values are reported in Supplementary Table 1.

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  Fig. 4. Schematic illustration of Tetranectin’s potential roles in Rotator Cuff Tear pathology. Elevated synovial tetranectin (CLEC3B) contributes to disease progression through three primary pathways: ECM breakdown and fibrinolysis promoting matrix turnover; chronic inflammation modulating immune responses; and adipogenesis driving fatty infiltration within the rotator cuff muscle. ECM extracellular matrix, IL-1β interleukin-1 beta, TNF-α, tumor necrosis factor-alpha.