Relative roles of TGF-β and IGFBP-5 in idiopathic pulmonary fibrosis

A. Sureshbabu, E. Tonner, G. J. Allan, D. J. Flint

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Although most evident in the skin, the process of scarring, or fibrosis, occurs in all major organs because of impaired epithelial self-renewal. No current therapy exists for Idiopathic pulmonary fibrosis. The major profibrotic factor is TGF-β1 and developing inhibitors is an area of active research. Recently, IGFBP-5 has also been identified as a profibrotic factor, and studies suggest that, while both TGF-β1 and IGFBP-5 activate mesenchymal cells to increase collagen and fibronectin production, their effects on epithelial cells are distinct. TGF-β1 induces cell death and/or EMT in the epithelial cells, exacerbating the disruption of tissue architecture. In contrast, IGFBP-5 induces epithelial cell spreading over collagen or fibronectin matrices, increases secretion of laminin, the epithelial basement membrane, and enhances the survival of epithelial cells in nutrient-poor conditions, as exists in scar tissue. Thus, IGFBP-5 may enhance repair and may be an important target for antifibrotic therapies.
LanguageEnglish
Article number517687
Number of pages6
JournalPulmonary Medicine
Volume2011
DOIs
Publication statusPublished - 2011

Fingerprint

Insulin-Like Growth Factor Binding Protein 5
Idiopathic Pulmonary Fibrosis
Transforming Growth Factor beta
Epithelial Cells
Fibronectins
Cicatrix
Collagen
Laminin
Basement Membrane
Fibrosis
Cell Death
Food
Skin
Therapeutics
Research

Keywords

  • scarring
  • fibrosis
  • epithelial self-renewal
  • pulmonary fibrosis
  • TGF-β1
  • IGFBP-5
  • idiopathic pulmonary fibrosis

Cite this

Sureshbabu, A. ; Tonner, E. ; Allan, G. J. ; Flint, D. J. / Relative roles of TGF-β and IGFBP-5 in idiopathic pulmonary fibrosis. In: Pulmonary Medicine. 2011 ; Vol. 2011.
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Relative roles of TGF-β and IGFBP-5 in idiopathic pulmonary fibrosis. / Sureshbabu, A.; Tonner, E.; Allan, G. J.; Flint, D. J.

In: Pulmonary Medicine, Vol. 2011, 517687, 2011.

Research output: Contribution to journalArticle

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AU - Allan, G. J.

AU - Flint, D. J.

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AB - Although most evident in the skin, the process of scarring, or fibrosis, occurs in all major organs because of impaired epithelial self-renewal. No current therapy exists for Idiopathic pulmonary fibrosis. The major profibrotic factor is TGF-β1 and developing inhibitors is an area of active research. Recently, IGFBP-5 has also been identified as a profibrotic factor, and studies suggest that, while both TGF-β1 and IGFBP-5 activate mesenchymal cells to increase collagen and fibronectin production, their effects on epithelial cells are distinct. TGF-β1 induces cell death and/or EMT in the epithelial cells, exacerbating the disruption of tissue architecture. In contrast, IGFBP-5 induces epithelial cell spreading over collagen or fibronectin matrices, increases secretion of laminin, the epithelial basement membrane, and enhances the survival of epithelial cells in nutrient-poor conditions, as exists in scar tissue. Thus, IGFBP-5 may enhance repair and may be an important target for antifibrotic therapies.

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