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Updated: Apr 25, 2026

Micro-Mechanical Characterization of Lung Tissue Using Atomic Force Microscopy
Published on: August 28, 2011
Versican regulating viscoelasticity drives pleural fibrosis via mechanotransductive signaling
Zi-Heng Jia1, Xin-Liang He1,2, Xiao-Lin Cui3
1Department of Respiratory and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Abstract:
Extracellular matrix (ECM) disorder was believed to result from fibrosis, but it has recently been recognized that fibrotic ECM initiates a self-reinforcing circuit and contributes to the development of fibrosis. Versican, an ECM component, participates in cell-ECM interaction and ECM regeneration. In pleura, versican is primarily derived from pleural mesothelial cells (PMCs). However, the role and mechanism of versican in pleural fibrosis has remained unknown. In this study, versican and versican-mediated pleural viscoelasticity were found to be elevated in both human and murine pleural fibrotic tissues. Versican knockdown by shRNA prevented increases in viscoelasticity as well as pleural fibrosis. High levels of versican and viscoelasticity promoted mesothelial-mesenchymal transition in PMCs. Mechanistically, increased viscoelasticity induced pleural fibrosis through the CD44/USP10/Smad4 mechanotransduction pathway. In conclusion, these results revealed that excessive versican in fibrotic pleural ECM enhanced ECM viscoelasticity and consequently promoted progression of pleural fibrosis.
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