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. Author manuscript; available in PMC: 2016 Mar 16.
Published in final edited form as: Cell Rep. 2016 Mar 3;14(10):2325–2336. doi: 10.1016/j.celrep.2016.02.029

Figure 2. Oncogenic Kras induces ADM through generation of mitochondrial oxidative stress.

Figure 2

A: Primary mouse pancreatic acinar cells were isolated from wildtype mice, infected with lentivirus harboring control (null) or KrasG12V, and then seeded in 3D collagen explant culture in presence of the ROS scavenger N-Acetyl-Cysteine (NAC, 5 mM). At day 5, bright field pictures were taken (4x magnification, show is a representative picture) and ducts formed (ADM events; number of ducts per field) were counted. The bar indicates 100 μm. B: Primary mouse pancreatic acinar cells were isolated from wildtype mice, double-infected with adeno-null (control, empty virus) or adeno-mCatalase (catalase targeted to the mitochondria), and lentivirus harboring control (null) or KrasG12V. Cells were then seeded in 3D collagen explant culture. At day 5, brightfield pictures were taken (4x magnification, show is a representative picture) and ducts formed (ADM events; number of ducts per field) were counted. The bar indicates 100 μm. C: Primary mouse pancreatic acinar cells were isolated from wildtype mice, infected with lentivirus harboring control (null) or KrasG12V, and then seeded in 3D collagen explant culture in presence of the mitochondria-targeted antioxidant mitoQ (500 nM). At day 5, bright field pictures were taken (4x magnification, show is a representative picture) and ducts formed (ADM events; number of ducts per field) were counted. The bar indicates 100 μm. In A–C, * indicates statistical significance (p<0.05) as compared to control; ** as compared to KrasG12V.