Skip to main content
. Author manuscript; available in PMC: 2013 Sep 15.
Published in final edited form as: Cancer Res. 2013 Jan 23;73(6):1721–1732. doi: 10.1158/0008-5472.CAN-12-2233

Figure 1.

Figure 1

LOX is critical for the development of a fibrotic microenvironment following injury

(A) Ashcroft scores representing the extent of fibrosis in lungs of control, bleomycin-treated, and irradiated mice. (B) Sirius Red staining (parallel light) of pulmonary tissue from control, bleomycin-treated and irradiated lung tissue. Fibrosis is highlighted by increased collagen deposition, significant disorganized thickening of alveolar septae, loss of normal alveolar architecture and considerable obstruction of alveoli due to collapse of alveolar space. (Scale bar = approx 50μm). (C) Increased collagen deposition in bleomycin-treated and irradiated pulmonary tissue as determined by SirCol quantification. (D) Immunofluorescence of control, bleomycin-treated and irradiated pulmonary tissue for LOX (alexafluor: green) shows increased levels of expression during fibrosis. (Scale bar = approx 50μm) (E) Quantitative analysis of LOX expression from immunofluorescence based on signal intensity measured using ImageJ. (F) Immunoblot analysis of LOX protein levels confirms elevated expression in both bleomycin-treated and irradiated pulmonary tissue following exposure compared to control. (G) Rising pulmonary collagen deposition in bleomycin-treated pulmonary tissue over time as determined by SirCol quantification (n = 3 mice per group).