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. 2013 May;182(5):1572–1584. doi: 10.1016/j.ajpath.2013.01.026

Figure 4.

Figure 4

FRNK deficiency potentiates, and FRNK restoration abrogates, TGF-β1–induced fibrotic responses in murine lung fibroblasts. A: Murine lung fibroblasts were derived from FRNK−/− and WT mice, and infected with adenoviral vector expressing either FRNK (Ad-FRNK) or control GFP (Ad-GFP). Cell migration in response to 10 ng/mL TGF-β1 in serum-free medium with 1% BSA (SFM) was examined by wound closure assay. Data are pooled and shown as % of wound area covered by cells over 24 hours, relative to that of uninfected WT fibroblasts in SFM medium. Data are given as means ± SE. B and C: FRNK−/− and WT lung fibroblasts were infected with Ad-FRNK or control Ad-GFP, followed by 10 ng/mL TGF-β1 treatment (for 36 hours) or vehicle. Equivalent amounts of whole cell lysates underwent Western blot analysis with indicated antibodies. FN, fibronectin; Pro-Col, procollagen 1. GAPDH was used as the loading control. D: FRNK−/− and WT lung fibroblasts were infected with Ad-FRNK or control Ad-GFP, followed by 10 ng/mL TGF-β1 treatment or vehicle and subjected to the collagen gel contraction assays for 50 hours. The ratio of collagen gel area after contraction against the original collagen gel area (before contraction) was calculated. Data are presented as the percentage of gel area relative to control (vehicle only, set as 100%). ∗P < 0.01.