Fibrosis involves activation of fibroblasts, increased production of collagen and fibronectin and transdifferentiation into contractile myofibroblasts. The process resembles aspects of wound-healing but remains unresolved and can be life-threatening when manifest in the kidneys, lungs and liver, in particular. The causes are largely unknown, but recent suggestions that repetitive micro-injury results in the eventual failure of epithelial cell repair due to replicative senescence are gaining favour. This is consistent with the onset of fibrotic diseases in middle age. Because epithelial injury often involves blood loss, inflammatory responses associated with the fibrotic response have been considered as therapeutic targets. However, this has proved largely unsuccessful and focus is now switching to earlier events in the process. These include EMT (epithelial–mesenchymal transition) and fibroblast activation in the absence of inflammation. TGFβ1 (transforming growth factor-β1) induces both EMT and fibroblast activation and is considered to be a major pro-fibrotic factor. Recently, IGFBP-5 [IGF (insulin-like growth factor)-binding protein-5] has also been shown to induce similar effects on TGFβ1, and is strongly implicated in the process of senescence. It also stimulates migration of peripheral blood mononuclear cells, implicating it in the inflammatory response. In this paper, we examine the evidence for a role of IGFBP-5 in fibrosis and highlight its structural relationship with other matrix proteins and growth factors also implicated in tissue remodelling.
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August 2009
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Conference Article|
July 22 2009
IGFBP-5 induces epithelial and fibroblast responses consistent with the fibrotic response
Angara Sureshbabu;
Angara Sureshbabu
*SIPBS, Strathclyde University, Glasgow G4 0NR, U.K.
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Hiroshi Okajima;
Hiroshi Okajima
†Graduate School of Agriculture and Life Sciences, University of Tokyo, Tokyo, Japan
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Daisuke Yamanaka;
Daisuke Yamanaka
†Graduate School of Agriculture and Life Sciences, University of Tokyo, Tokyo, Japan
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Surya Shastri;
Surya Shastri
*SIPBS, Strathclyde University, Glasgow G4 0NR, U.K.
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Elizabeth Tonner;
Elizabeth Tonner
*SIPBS, Strathclyde University, Glasgow G4 0NR, U.K.
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Colin Rae;
Colin Rae
*SIPBS, Strathclyde University, Glasgow G4 0NR, U.K.
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Malgorzata Szymanowska;
Malgorzata Szymanowska
*SIPBS, Strathclyde University, Glasgow G4 0NR, U.K.
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John H. Shand;
John H. Shand
*SIPBS, Strathclyde University, Glasgow G4 0NR, U.K.
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Shin-Ichiro Takahashi;
Shin-Ichiro Takahashi
†Graduate School of Agriculture and Life Sciences, University of Tokyo, Tokyo, Japan
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James Beattie;
James Beattie
‡Department of Oral Biology, Leeds Dental Institute, University of Leeds, Leeds LS2 9LU, U.K.
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Gordon J. Allan;
Gordon J. Allan
*SIPBS, Strathclyde University, Glasgow G4 0NR, U.K.
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David J. Flint
David J. Flint
1
*SIPBS, Strathclyde University, Glasgow G4 0NR, U.K.
1To whom correspondence should be addressed (email david.flint@strath.ac.uk).
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Publisher: Portland Press Ltd
Received:
March 03 2009
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© The Authors Journal compilation © 2009 Biochemical Society
2009
Biochem Soc Trans (2009) 37 (4): 882–885.
Article history
Received:
March 03 2009
Citation
Angara Sureshbabu, Hiroshi Okajima, Daisuke Yamanaka, Surya Shastri, Elizabeth Tonner, Colin Rae, Malgorzata Szymanowska, John H. Shand, Shin-Ichiro Takahashi, James Beattie, Gordon J. Allan, David J. Flint; IGFBP-5 induces epithelial and fibroblast responses consistent with the fibrotic response. Biochem Soc Trans 1 August 2009; 37 (4): 882–885. doi: https://doi.org/10.1042/BST0370882
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