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Investigates SPARC's role in inflammation and adhesion formation in mice, suggesting potential targets for treatment.
Postoperative abdominal adhesions can cause several complications, such as intestinal obstruction, female infertility, and chronic pelvic pain. By alkaline cauterization of the cecum, we established a mouse abdominal adhesion model to investigate the roles of secreted protein acidic and rich in cysteine (SPARC) in adhesion formation. Alkaline cauterization led to elevation of adhesion scores and mRNA levels of SPARC, monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-α (TNF-α), and collagen I on Days 3, 7, and 14, with a positive correlation between SPARC levels and MCP-1, TNF-α, and collagen I during Days 3-14. Histological assessment revealed the presence of fibrillar collagen in the adhesive tissue between the cecum and other organs/tissues and SPARC at the fibrotic sites. Matrix metalloproteinase (MMP)-9 and MMP-2 were upregulated in the adhesion group on Days 3-7 and 7-14, respectively, with these expressions correlating with SPARC on Days 3, 7, and 14. A disintegrin and metalloproteinase with thrombospondin type 1 motif (ADAMTS1), which colocalized with SPARC, was increased in the adhesion model, and showed a positive correlation with SPARC, MCP-1, TNF-α, and collagen I on Days 3 and 7, but not on Day 14. In conclusion, SPARC induction might play important roles in adhesion formation and development.
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Toba et al. (2026) studied this question.
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