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<p>The activation and accumulation of lung fibroblasts, leading to excessive ECM deposition, is a pathogenic hallmark of Idiopathic Pulmonary Fibrosis, a lethal and currently untreatable disease. In this report, increased expression of Versican, a multifunctional ECM proteoglycan, is detected in both human and mouse pulmonary fibrosis, mainly in monocytic cells and fibroblasts. Ubiquitous genetic reduction of Versican expression in mice promotes collagen expression and polymerisation, alters pulmonary ECM composition and structure, and exacerbates pulmonary fibrosis, delaying its resolution. Moreover, the decrease in Versican in the ECM and the ensuing reorganisation stimulate Tenascin-C expression from fibroblasts, which is further shown to be a potent Toll-like receptor 4-dependent podosome inducer, promoting ECM invasion. Thus, fibroblast-expressed Versican regulates the underlying ECM composition and structure and suppresses autologous podosome formation, limiting ECM invasion and pulmonary fibrosis.</p>

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Versican expression from lung fibroblasts suppresses pulmonary fibrosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月21日

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  • Paraskevi Kanellopoulou,
  • Ilianna Barbayianni,
  • Dionysios Fanidis,
  • Martina Samiotaki,
  • Eleni Katsiouli,
  • Dimitris Nastos,
  • Stefanos Smyrniotis,
  • Maria Shira,
  • Apostolos Galaris,
  • Vagelis Rinotas,
  • Sofia Grammenoudi,
  • Christiana Magkrioti,
  • Ioannis Tomos,
  • Africa Martinez Blanco,
  • Ioanna Tremi,
  • Ioannis Vamvakaris,
  • Nuria Gavara,
  • Sophia Havaki,
  • Vassilis Gorgoulis,
  • Hideto Watanabe,
  • Vassilis Aidinis

摘要

The activation and accumulation of lung fibroblasts, leading to excessive ECM deposition, is a pathogenic hallmark of Idiopathic Pulmonary Fibrosis, a lethal and currently untreatable disease. In this report, increased expression of Versican, a multifunctional ECM proteoglycan, is detected in both human and mouse pulmonary fibrosis, mainly in monocytic cells and fibroblasts. Ubiquitous genetic reduction of Versican expression in mice promotes collagen expression and polymerisation, alters pulmonary ECM composition and structure, and exacerbates pulmonary fibrosis, delaying its resolution. Moreover, the decrease in Versican in the ECM and the ensuing reorganisation stimulate Tenascin-C expression from fibroblasts, which is further shown to be a potent Toll-like receptor 4-dependent podosome inducer, promoting ECM invasion. Thus, fibroblast-expressed Versican regulates the underlying ECM composition and structure and suppresses autologous podosome formation, limiting ECM invasion and pulmonary fibrosis.