Skip to main content
. 2010 Oct 11;120(11):3969–3978. doi: 10.1172/JCI42563

Figure 8. Transgenic coexpression of the inflammatory chemokine CCL2 exacerbates the phenotype of VS28L18 mice.

Figure 8

The inflammatory chemokine CCL2 is an agonist for US28. To test whether CCL2 can activate US28 in vivo, we generated mice expressing both CCL2 and US28 in IECs. (A) Generation of mice expressing both CCL2 and US28 in IECs (V2S28 mice). A 9-kb fragment of the villin promoter was used to drive expression of mouse CCL2 (mCCL2) to IECs (VCCL2 mice). Subsequently, the VCCL2 transgenic mice were crossed with VS28L18 mice to generate V2S28 mice. (B) CCL2 and US28 mRNA expression in the jejunum of WT, VCCL2, VS28L18, and V2S28 mice. Values were standardized to ubiquitin (n = 3). (C–E) H&E staining of the jejunum of VS28L18 (C), VCCL2 (D), and V2S28 mice (E). (F) Analysis of BrdU+ incorporation in CD45– IECs from the jejunum of WT, VCCL2, VS28L18, and V2S28 mice was determined using FACS analysis (n = 4 mice per group). *P < 0.05, ***P < 0.001 vs. WT. #P < 0.05, ##P < 0.01 vs. VS28L18. (G) H&E-stained section of jejunal tubular adenoma found in a V2S28 mouse. Scale bar: 100 μm (C–E and G). Results represent the mean ± SEM.