The matrix protein Fibulin-5 is at the interface of tissue stiffness and inflammation in fibrosis

Manando Nakasaki, Yongsung Hwang, Yun Xie, Sunny Kataria, Rupali Gund, Edries Y. Hajam, Rekha Samuel, Renu George, Debashish Danda, Paul M.J., Tomoyuki Nakamura, Zhouxin Shen, Steve Briggs, Shyni Varghese () and Colin Jamora ()
Additional contact information
Manando Nakasaki: IFOM-inSTEM Joint Research Laboratory, Centre for Inflammation and Tissue Homeostasis (inStem), NCBS GKVK Post
Yongsung Hwang: University of California, San Diego
Yun Xie: University of California, San Diego
Sunny Kataria: IFOM-inSTEM Joint Research Laboratory, Centre for Inflammation and Tissue Homeostasis (inStem), NCBS GKVK Post
Rupali Gund: IFOM-inSTEM Joint Research Laboratory, Centre for Inflammation and Tissue Homeostasis (inStem), NCBS GKVK Post
Edries Y. Hajam: IFOM-inSTEM Joint Research Laboratory, Centre for Inflammation and Tissue Homeostasis (inStem), NCBS GKVK Post
Rekha Samuel: Center for Stem Cell Research, Christian Medical College
Renu George: Venereology and Leprosy, Christian Medical College
Debashish Danda: Christian Medical College
Paul M.J.: Christian Medical College
Tomoyuki Nakamura: Kansai Medical University
Zhouxin Shen: Section of Cell and Developmental Biology, University of California, San Diego
Steve Briggs: Section of Cell and Developmental Biology, University of California, San Diego
Shyni Varghese: University of California, San Diego
Colin Jamora: IFOM-inSTEM Joint Research Laboratory, Centre for Inflammation and Tissue Homeostasis (inStem), NCBS GKVK Post

Nature Communications, 2015, vol. 6, issue 1, 1-11

Abstract: Abstract Fibrosis is a pervasive disease in which the excessive deposition of extracellular matrix (ECM) compromises tissue function. Although the underlying mechanisms are mostly unknown, matrix stiffness is increasingly appreciated as a contributor to fibrosis rather than merely a manifestation of the disease. Here we show that the loss of Fibulin-5, an elastic fibre component, not only decreases tissue stiffness, but also diminishes the inflammatory response and abrogates the fibrotic phenotype in a mouse model of cutaneous fibrosis. Increasing matrix stiffness raises the inflammatory response above a threshold level, independent of TGF-β, to stimulate further ECM secretion from fibroblasts and advance the progression of fibrosis. These results suggest that Fibulin-5 may be a therapeutic target to short-circuit this profibrotic feedback loop.

Date: 2015
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DOI: 10.1038/ncomms9574

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