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Elevated expression of galectin-3 in excessive scars: A pilot study

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  • Additional Information
    • Publication Information:
      Sociedade Brasileira de Cirurgia Plástica, 2024.
    • Publication Date:
      2024
    • Collection:
      LCC:Surgery
    • Abstract:
      Introduction: Hypertrophic scars and keloids are types of excessive scars from abnormal skin healing. Galectin-3 (gal-3) is a protein from the lectin family capable of identifying carbohydrates, which can combine and act on different molecules. In the literature, the action of gal-3 as the main regulatory agent of fibrogenesis has already been described and is currently used in anti-fibrotic therapy for various organs such as the lung and liver. The objective of this pilot study was to show preliminary results found in the expression of gal-3 in exacerbated scars. Method: Twenty biopsy samples from excessive scars (16 keloids and 4 hypertrophic scars) and 9 samples from normal scars were collected from 22 women and 7 men. These samples were processed for routine histopathological analysis by immunohistochemistry to detect gal-3. Gal-3 positive cells were quantified by the stereological method using a 36-point grid. Results: Immunohistochemistry showed high expression of gal-3 in endothelial and epithelial cells of all scar samples, as well as expression in cells distributed throughout the dermis. Higher gal-3 expression was found in keloid samples (28% positive cells) compared to normal (18%) and hypertrophic (22%) scars (p = 0.0075). The results were obtained from a small number of patients, as this was a pilot study. Conclusion: The data suggest that gal-3 participates in the healing process and, due to its greater presence in keloid samples, it may be a potential biomarker for keloid formation and a promising therapeutic target to be explored.
    • File Description:
      electronic resource
    • ISSN:
      1983-5175
      2177-1235
    • Relation:
      http://www.rbcp.org.br/export-pdf/3482/1983-5175-rbcp-39-03-e936-en.pdf; https://doaj.org/toc/1983-5175; https://doaj.org/toc/2177-1235
    • Accession Number:
      10.5935/2177-1235.2024RBCP0936-EN
    • Accession Number:
      edsdoj.80c4b60552e64732abe4d43f4f46b6b1