Decreased tissue and serum expression of galectin-7 in patients with hypertrophic scars.

Acta Derm Venereol

Department of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine 250 Seongsanno, Seodaemoon-gu, Seoul, 120-752, Korea.

Published: November 2013

AI Article Synopsis

  • Hypertrophic scars (HS) occur due to an imbalance in collagen production during wound healing, leading to changes in protein profiles in skin tissue.
  • The protein galectin-7 was found to be significantly lower in patients with HS compared to healthy individuals, both in serum and tissue samples.
  • The study indicates that the differences in galectin-7 levels and distribution in HS tissue might play an important role in the development of these scars.

Article Abstract

Hypertrophic scars (HS) result from an imbalance between collagen biosynthesis and matrix degradation during wound healing. In this study a proteomics approach was used to compare the protein profiles of skin tissue obtained from patients with HS and healthy controls. One of the epidermal proteins, galectin-7 was markedly down-regulated in HS. Serum levels of galectin-7 in 27 patients with HS were less than 1/3 of those in 15 healthy controls. Tissue protein expression was subsequently evaluated using immunohistochemical staining on HS tissue and on serially-obtained control tissue during wound healing. Weaker galectin-7 immunoreactivity was detected along the cytoplasmic membrane of basal and suprabasal cells in samples from HS. In addition, galectin-7 was stained in the extracellular space of the upper papillary dermis in HS tissue. Ablative laser treatment, used to induce wound healing of healthy control tissue, demonstrated marked galectin-7 expression at the cytoplasmic membrane on days 3, 5, 14 and 21. Pronounced galectin-7 staining at the upper papillary dermis was detected on days 1, 3 and 10. These results suggest that the differences in galectin-7 expression and subcellular and extracellular distribution may be crucially involved in the pathogenic process of HS.

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Source
http://dx.doi.org/10.2340/00015555-1583DOI Listing

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