JCI table of contents November 1, 2004

duced fibrosis to determine if it is mediated through the action of c-Abl, which is already known to mediate PDGF action. The authors show that c-Abl is a direct target of TGF-b and that its kinase activity is stimulated by TGF-b in a Smad2/3-independent manner. Further, TGF-b stimulation of c-Abl kinase activity did not require PDGFR phosphorylation or expression. Use of imatinib, an FDA-approved treatment for chronic myelogenous leukemia that inhibits c-Abl family kinases, blocked TGF-binduced fibroblast morphological changes and proliferation in culture. In vivo, imatinib treatment in a bleomycin-induced pulmonary fibrosis mouse model resulted in reduced collagen deposition and tissue destruction in addition to a lower number of inflammatory cells in lung tissue compared with that found in untreated mice. This study provides evidence that c-Abl family members may be primary targets of profibrotic cytokine signaling and that imatinib represents a potentially effective in vivo therapy for growth-dependent fibrosis in an animal model.

TITLE: Imatinib mesylate inhibits the profibrogenic activity of TGF-b and prevents bleomycin-mediated lung fibrosis

Edward B. Leof
Mayo Clinic, Rochester, MN 55905, USA
Phone: 507-284-5717; Fax: 507-284-4521; E-mail: leof.edward@mayo.edu

View the PDF of this article at: https://www.the-jci.org/press/19603.pdf

Gene that Inhibits Cancer Metastasis Identified

Melanoma is the deadliest form of skin cancer, primarily because of its highly metastatic nature. One class of proteins called semaphorins could play a role in the development of tumor metastasis as they have been shown to block the migration of some cell types in culture. Michael Klagsbrun and colleagues, from Harvard Medical School, examined semaphorin 3F (SEMA3F) expression in human metastatic

Contact: Laurie Goodman
Journal of Clinical Investigation

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