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. 2013 Apr 8;123(5):2231–2243. doi: 10.1172/JCI64498

Figure 1. Loss of pancreatic IKKα results in spontaneous and progressive pancreatitis.

Figure 1

(A) IB analysis of pancreas (P) or liver (L) lysates of IkkαF/F and IkkαΔpan mice. (B–J) Histological analysis of pancreatic sections from IkkαF/F and IkkαΔpan mice. H&E staining of pancreatic sections (B, D, and E). Note acinar cell vacuolization (C, arrows), ductal metaplasia (F), BrdU incorporation in active ductal metaplasia (G), immune cell infiltration (H), fat tissue replacement (I), and condensed luminal contents in dilated ducts (J) in IkkαΔpan pancreata. Original magnification, ×200 (B, C, D, E, and I); ×400 (F, G, H, and J). (K) Sirius red staining showing pancreatic fibrosis in 3-month-old IkkαΔpan mice. Original magnification, ×200. (L and M) qRT-PCR analysis of pancreatic RNAs from 3-month-old mice for fibrogenic markers (L) and cytokine and chemokine genes and immune cell markers (M). Results are shown as mean ± SEM. n = 4–6 mice per condition. *P < 0.05; **P < 0.01. Scale bars: 50 μm; 20 μm (insets).