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(American Journal of Pathology. 2005;166:1321-1332.)
© 2005 American Society for Investigative Pathology

Induction of Epithelial-Mesenchymal Transition in Alveolar Epithelial Cells by Transforming Growth Factor-ß1

Potential Role in Idiopathic Pulmonary Fibrosis

Brigham C. Willis*{dagger}{ddagger}, Janice M. Liebler{dagger}, Katherine Luby-Phelps§, Andrew G. Nicholson, Edward D. Crandall{dagger}, Roland M. du Bois and Zea Borok{dagger}

From the Department of Anesthesiology Critical Care Medicine,* Childrens Hospital Los Angeles, Los Angeles, California; the Division of Pulmonary and Critical Care Medicine,{dagger} Will Rogers Institute Pulmonary Research Center, Keck School of Medicine, University of Southern California, Los Angeles, California; the Division of Pediatric Critical Care Medicine,{ddagger} Department of Pediatrics, and the Department of Cell Biology,§ University of Texas Southwestern Medical School, Dallas, Texas; and Royal Brompton Hospital, Sydney Street, London, United Kingdom

The hallmark of idiopathic pulmonary fibrosis (IPF) is the myofibroblast, the cellular origin of which in the lung is unknown. We hypothesized that alveolar epithelial cells (AECs) may serve as a source of myofibroblasts through epithelial-mesenchymal transition (EMT). Effects of chronic exposure to transforming growth factor (TGF)-ß1 on the phenotype of isolated rat AECs in primary culture and a rat type II cell line (RLE-6TN) were evaluated. Additionally, tissue samples from patients with IPF were evaluated for cells co-expressing epithelial (thyroid transcription factor (TTF)-1 and pro-surfactant protein-B (pro-SP-B), and mesenchymal ({alpha}-smooth muscle actin ({alpha}-SMA)) markers. RLE-6TN cells exposed to TGF-ß1 for 6 days demonstrated increased expression of mesenchymal cell markers and a fibroblast-like morphology, an effect augmented by tumor necrosis factor-{alpha} (TNF-{alpha}). Exposure of rat AECs to TGF-ß1 (100 pmol/L) resulted in increased expression of {alpha}-SMA, type I collagen, vimentin, and desmin, with concurrent transition to a fibroblast-like morphology and decreased expression of TTF-1, aquaporin-5 (AQP5), zonula occludens-1 (ZO-1), and cytokeratins. Cells co-expressing epithelial markers and {alpha}-SMA were abundant in lung tissue from IPF patients. These results suggest that AECs undergo EMT when chronically exposed to TGF-ß1, raising the possibility that epithelial cells may serve as a novel source of myofibroblasts in IPF.




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C. Bianco, L. Strizzi, M. Mancino, A. Rehman, S. Hamada, K. Watanabe, A. De Luca, B. Jones, G. Balogh, J. Russo, et al.
Identification of Cripto-1 as a Novel Serologic Marker for Breast and Colon Cancer
Clin. Cancer Res., September 1, 2006; 12(17): 5158 - 5164.
[Abstract] [Full Text] [PDF]

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 Proc. Natl. Acad. Sci. USAHome page
K. K. Kim, M. C. Kugler, P. J. Wolters, L. Robillard, M. G. Galvez, A. N. Brumwell, D. Sheppard, and H. A. Chapman
Alveolar epithelial cell mesenchymal transition develops in vivo during pulmonary fibrosis and is regulated by the extracellular matrix
PNAS, August 29, 2006; 103(35): 13180 - 13185.
[Abstract] [Full Text] [PDF]

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 ChestHome page
R. M. du Bois
Fibroblastic foci: time to be counted?
Chest, July 1, 2006; 130(1): 3 - 5.
[Full Text] [PDF]

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 Am. J. Pathol.Home page
K. Koli, M. Myllarniemi, K. Vuorinen, K. Salmenkivi, M. J. Ryynanen, V. L. Kinnula, and J. Keski-Oja
Bone Morphogenetic Protein-4 Inhibitor Gremlin Is Overexpressed in Idiopathic Pulmonary Fibrosis
Am. J. Pathol., July 1, 2006; 169(1): 61 - 71.
[Abstract] [Full Text] [PDF]

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 J. Cell Sci.Home page
B. Cat, D. Stuhlmann, H. Steinbrenner, L. Alili, O. Holtkotter, H. Sies, and P. Brenneisen
Enhancement of tumor invasion depends on transdifferentiation of skin fibroblasts mediated by reactive oxygen species
J. Cell Sci., July 1, 2006; 119(13): 2727 - 2738.
[Abstract] [Full Text] [PDF]

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 Am. J. Respir. Crit. Care Med.Home page
F. J. Martinez and M. P. Keane
Update in diffuse parenchymal lung diseases 2005.
Am. J. Respir. Crit. Care Med., May 15, 2006; 173(10): 1066 - 1071.
[Full Text] [PDF]

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 Am. J. Respir. Cell Mol. Bio.Home page
I. S. Douglas, F. D. del Valle, R. A. Winn, and N. F. Voelkel
beta-Catenin in the Fibroproliferative Response to Acute Lung Injury
Am. J. Respir. Cell Mol. Biol., March 1, 2006; 34(3): 274 - 285.
[Abstract] [Full Text] [PDF]

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 Am. J. Respir. Crit. Care Med.Home page
V. J. Thannickal and A. U. Wells
Classification of Interstitial Pneumonias: What Do Gene Expression Profiles Tell Us?
Am. J. Respir. Crit. Care Med., January 15, 2006; 173(2): 141 - 142.
[Full Text] [PDF]

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 Am. J. Respir. Crit. Care Med.Home page
M. Selman, A. Pardo, L. Barrera, A. Estrada, S. R. Watson, K. Wilson, N. Aziz, N. Kaminski, and A. Zlotnik
Gene Expression Profiles Distinguish Idiopathic Pulmonary Fibrosis from Hypersensitivity Pneumonitis
Am. J. Respir. Crit. Care Med., January 15, 2006; 173(2): 188 - 198.
[Abstract] [Full Text] [PDF]

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 Proc Am Thorac SocHome page
V. J. Thannickal and J. C. Horowitz
Evolving concepts of apoptosis in idiopathic pulmonary fibrosis.
Proceedings of the ATS, January 1, 2006; 3(4): 350 - 356.
[Abstract] [Full Text] [PDF]

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 Proc Am Thorac SocHome page
M. Selman and A. Pardo
Role of epithelial cells in idiopathic pulmonary fibrosis: from innocent targets to serial killers.
Proceedings of the ATS, January 1, 2006; 3(4): 364 - 372.
[Abstract] [Full Text] [PDF]

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 Proc Am Thorac SocHome page
B. C. Willis, R. M. duBois, and Z. Borok
Epithelial Origin of Myofibroblasts during Fibrosis in the Lung.
Proceedings of the ATS, January 1, 2006; 3(4): 377 - 382.
[Abstract] [Full Text] [PDF]

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 Proc Am Thorac SocHome page
K. Ask, G. E. M. Martin, M. Kolb, and J. Gauldie
Targeting genes for treatment in idiopathic pulmonary fibrosis: challenges and opportunities, promises and pitfalls.
Proceedings of the ATS, January 1, 2006; 3(4): 389 - 393.
[Abstract] [Full Text] [PDF]


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