The mTORC1/4E-BP1 axis represents a critical signaling node during fibrogenesis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-12

AUTHORS

Hannah V. Woodcock, Jessica D. Eley, Delphine Guillotin, Manuela Platé, Carmel B. Nanthakumar, Matteo Martufi, Simon Peace, Gerard Joberty, Daniel Poeckel, Robert B. Good, Adam R. Taylor, Nico Zinn, Matthew Redding, Ellen J. Forty, Robert E. Hynds, Charles Swanton, Morten Karsdal, Toby M. Maher, Giovanna Bergamini, Richard P. Marshall, Andy D. Blanchard, Paul F. Mercer, Rachel C. Chambers

ABSTRACT

Myofibroblasts are the key effector cells responsible for excessive extracellular matrix deposition in multiple fibrotic conditions, including idiopathic pulmonary fibrosis (IPF). The PI3K/Akt/mTOR axis has been implicated in fibrosis, with pan-PI3K/mTOR inhibition currently under clinical evaluation in IPF. Here we demonstrate that rapamycin-insensitive mTORC1 signaling via 4E-BP1 is a critical pathway for TGF-β1 stimulated collagen synthesis in human lung fibroblasts, whereas canonical PI3K/Akt signaling is not required. The importance of mTORC1 signaling was confirmed by CRISPR-Cas9 gene editing in normal and IPF fibroblasts, as well as in lung cancer-associated fibroblasts, dermal fibroblasts and hepatic stellate cells. The inhibitory effect of ATP-competitive mTOR inhibition extended to other matrisome proteins implicated in the development of fibrosis and human disease relevance was demonstrated in live precision-cut IPF lung slices. Our data demonstrate that the mTORC1/4E-BP1 axis represents a critical signaling node during fibrogenesis with potential implications for the development of novel anti-fibrotic strategies. More... »

PAGES

6

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41467-018-07858-8

DOI

http://dx.doi.org/10.1038/s41467-018-07858-8

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1110929188

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30602778


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