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(American Journal of Pathology. 2005;167:365-379.)
© 2005 American Society for Investigative Pathology

Loss of Fibroblast Thy-1 Expression Correlates with Lung Fibrogenesis

James S. Hagood*{dagger}, Priya Prabhakaran*, Pallavi Kumbla*, Lorena Salazar*, Mark W. MacEwen*, Thomas H. Barker{ddagger}, Luis A. Ortiz§, Trenton Schoeb, Gene P. Siegal{dagger}||**, C. Bruce Alexander||, Annie Pardo{dagger}{dagger} and Moisés Selman{ddagger}{ddagger}

From the Departments of Pediatrics,* Cell Biology,{dagger} Genomics and Pathobiology, Pathology,|| and Surgery,** University of Alabama, Birmingham, Alabama; the Department of Environmental and Occupational Health,§ Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania; the Laboratory of Regenerative Medicine and Pharmacobiology,{ddagger} Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland; the Facultad de Ciencias,{dagger}{dagger} Universidad Nacional Autónoma de México, Mexico City, Mexico; and the Instituto Nacional de Enfermedades Respiratorias,{ddagger}{ddagger} Mexico City, Mexico

Fibroblasts consist of heterogeneous subpopulations that have distinct roles in fibrotic responses. Previously we reported enhanced proliferation in response to fibrogenic growth factors and selective activation of latent transforming growth factor (TGF)-ß in fibroblasts lacking cell surface expression of Thy-1 glycoprotein, suggesting that Thy-1 modulates the fibrogenic potential of fibroblasts. Here we report that compared to controls Thy-1–/– C57BL/6 mice displayed more severe histopathological lung fibrosis, greater accumulation of lung collagen, and increased TGF-ß activation in the lungs 14 days after intratracheal bleomycin. The majority of cells demonstrating TGF-ß activation and myofibroblast differentiation in bleomycin-induced lesions were Thy-1-negative. Histological sections from patients with idiopathic pulmonary fibrosis demonstrated absent Thy-1 staining within fibroblastic foci. Normal lung fibroblasts, in both mice and humans, were predominantly Thy-1-positive. The fibrogenic cytokines interleukin-1 and tumor necrosis factor-{alpha} induced loss of fibroblast Thy-1 surface expression in vitro, which was associated with Thy-1 shedding, Smad phosphorylation, and myofibroblast differentiation. These results suggest that fibrogenic injury promotes loss of lung fibroblast Thy-1 expression, resulting in enhanced fibrogenesis.




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