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Transforming Growth Factor-β1 Modifies Fibroblast Growth Factor-2 Production in Type II Cells*

Cheng-Ming Li, MD, PhD; Jody Khosla, MSc; Paul Hoyle, PhD; Philip L. Sannes, PhD
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*From the Department of Anatomy, Physiological Sciences, and Radiology, North Carolina State University, Raleigh, NC.

Correspondence to: Philip L. Sannes, PhD, APR-NCSU CVM, 4700 Hillsborough St, Raleigh, NC 27606; e-mail: philip_sannes@ncsu.edu



Chest. 2001;120(1_suppl):S60-S61. doi:10.1378/chest.120.1_suppl.S60
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Transforming growth factor (TGF)-β1 is an inflammatory cytokine that plays multiple roles in pulmonary fibrosis. In vascular epithelium, it has been shown to regulate production and activity of fibroblast growth factor (FGF)-2, a potent type II cell mitogen in the lung. Such a relationship could have important consequences in prefibrotic change in the lung alveolus, where reepithelialization of alveolar surfaces is crucial. The goal of this study was to determine if FGF-2 production by alveolar type II cells is modulated by TGF-β1 or FGF-1, another type II cell mitogen. Isolated rat type II cells were exposed to 0 to 40 ng/mL of TGF-β1 or 0 to 500 ng/mL of FGF-1 in serum-free medium for 1 to 3 days. Using a specific immunoassay, significant increases in FGF-2 protein in type II cell lysates were achieved after 1 day of exposure to 100 ng/mL of FGF-1 and after 3 days of treatment with 8 ng/mL of TGF-β1. Similarly, transcripts for FGF-2 were dramatically increased with TGF-β1 or FGF-1, as were those for FGF receptor (FGFR)-1. These interactions were dramatically effected by the addition of heparin, a model sulfated extracellular matrix (ECM). Heparin as low as 0.01 mg/mL significantly downregulated expression of TGF-β1 and FGF-1–stimulated FGF-2 and FGFR-1. These results demonstrate important regulatory links between FGF-2, sulfated ECMs, and both TGF-β1 and FGF-1, which could contribute to the modulation of normal cell turnover, development, and repair processes attendant to fibrosis in the lung.


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