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. Author manuscript; available in PMC: 2008 May 5.
Published in final edited form as: J Invest Dermatol. 2007 May 31;127(11):2645–2655. doi: 10.1038/sj.jid.5700890

Figure 2. TNF-α suppresses TGF-β1 promotion of myofibroblast structural elements.

Figure 2

(a–d) Representative images of the immunohistochemistry staining for α-SMA. Normal human dermal fibroblasts (1 × 105 cells) were seeded in collagen I matrix (1 mg/ml), which remained attach to the culture plate throughout the cytokine stimulation period. α-SMA was visualized using mouse monoclonal α-SMA FITC conjugated. (a) FPCL under control conditions at 96 hours. (b) FPCL treated with TGF-β1 (1 ng/ml) for 96 hours. (c) FPCL treated with TNF-α (1 ng/ml), and (d) FPCL treated with combination of TGF-β1 (1 ng/ml) and TNF-α (1 ng/ml). Bars = 50 μm (panels a–d). (e–h) Rhodamine-conjugated phalloidin staining for F-actin to examine the assembly of stress fibers. (e) FPCL under control conditions at 96 hours. (f) FPCL treated with TGF-β1 (1 ng/ml) for 96 hours. (g) FPCL treated with TNF-α (1 ng/ml), and (h) FPCL treated with a combination of TGF-β1 (1 ng/ml) plus TNF-α (1 ng/ml). Bars = 50 μm (panels e–h).