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B64. PATHWAYS REGULATING FIBROBLAST GENE EXPRESSION - Insulin-Like Growth Factor Binding Protein-5 Promotes Fibrosis Through Modulation Of The Heat Shock Response by Veraldi, Kristen L.; Thiel, Katelynn J.; Feghali-Bostwick, Carol A. is a scholarly article available to read on EtoBox.

What is B64. PATHWAYS REGULATING FIBROBLAST GENE EXPRESSION - Insulin-Like Growth Factor Binding Protein-5 Promotes Fibrosis Through Modulation Of The Heat Shock Response about?

Interstitial Lung Disease comprises a number of disorders characterized by scarring, or fibrosis, of the lungs. We have RATIONALE: published the observation that insulin-like growth factor binding protein-5 (IGFBP-5) is a novel mediator of fibrosis that is increased in the lungs of individuals with idiopathic pulmonary fibrosis (IPF) and induces extracellular matrix (ECM) production by cultured primary lung fibroblasts and a fibrotic phenotype in an mouse model. Aberrant regulation of heat shock protein (Hsp) 70 kDa family members in vivo has been described in a number of human systemic diseases and in both rat and mouse models of acute lung injury. We now describe evidence to support our hypothesis that modulation of the heat shock response is one mechanism through which IGFBP-5 causes fibrosis. Expression of major Hsps was assayed at both the mRNA and protein level in lung tissue and cultured primary METHODS and RESULTS: lung fibroblasts from IPF versus normal (NL) controls, revealing decreased protein expression of the major stress-inducible isoform of the Hsp70 family (Hsp72) both in whole-lung homogenates and in primary lung fibroblasts from IPF. This difference was not presen

Author

Veraldi, Kristen L.; Thiel, Katelynn J.; Feghali-Bostwick, Carol A.

Publisher

American Thoracic Society

Published

2011

Language

EN