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<p>Keloid and morphea, although clinically distinct, share key pathological features characterized by aberrant wound healing and excessive extracellular matrix (ECM) deposition. Aggrecan, a large chondroitin sulfate proteoglycan predominantly found in cartilage, has recently been implicated in fibrotic disorders; however, its contribution to morphea pathogenesis remains unexplored. This study aimed to evaluate aggrecan expression and distribution in morphea and keloid tissues relative to normal skin, and to assess its potential involvement in fibrotic remodeling. Formalin-fixed, paraffin-embedded tissue samples from patients with morphea, keloid, hypertrophic scar, normal skin (negative control), and cartilage (positive control) were subjected to immunohistochemical staining using a monoclonal anti-aggrecan antibody. Staining intensity and distribution were semi-quantitatively assessed. Aggrecan expression was markedly increased in keloid and late-phase morphea lesions exhibiting advanced sclerosis, whereas no expression was observed in normal skin, hypertrophic scars, or early-phase morphea. Strong immunoreactivity in late-phase morphea correlated with pronounced dermal sclerosis and collagen condensation. These findings suggest that aggrecan contributes to the aberrant ECM accumulation characteristic of fibrotic skin diseases. Further mechanistic studies are warranted to elucidate its role in fibroblast activation and matrix remodeling during morphea progression.</p>

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Aggrecan expression in morphea tissues: a potential contributor to fibrotic extracellular matrix accumulation

  • 期刊论文

  • 发表日期：

    2026年7月11日

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  • Nilay Duman,
  • Banu Yaman,
  • Aslıhan Özel,
  • Mahdi Shekari,
  • Taner Akalın,
  • Özgür Çoğulu

摘要

Keloid and morphea, although clinically distinct, share key pathological features characterized by aberrant wound healing and excessive extracellular matrix (ECM) deposition. Aggrecan, a large chondroitin sulfate proteoglycan predominantly found in cartilage, has recently been implicated in fibrotic disorders; however, its contribution to morphea pathogenesis remains unexplored. This study aimed to evaluate aggrecan expression and distribution in morphea and keloid tissues relative to normal skin, and to assess its potential involvement in fibrotic remodeling. Formalin-fixed, paraffin-embedded tissue samples from patients with morphea, keloid, hypertrophic scar, normal skin (negative control), and cartilage (positive control) were subjected to immunohistochemical staining using a monoclonal anti-aggrecan antibody. Staining intensity and distribution were semi-quantitatively assessed. Aggrecan expression was markedly increased in keloid and late-phase morphea lesions exhibiting advanced sclerosis, whereas no expression was observed in normal skin, hypertrophic scars, or early-phase morphea. Strong immunoreactivity in late-phase morphea correlated with pronounced dermal sclerosis and collagen condensation. These findings suggest that aggrecan contributes to the aberrant ECM accumulation characteristic of fibrotic skin diseases. Further mechanistic studies are warranted to elucidate its role in fibroblast activation and matrix remodeling during morphea progression.