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1.
Figure 3

Figure 3. Intestinal mucosal thickening and cyst formation in vilVEGF mice. From: Transgenic Expression of VEGF in Intestinal Epithelium Drives Mesenchymal Cell Interactions and Epithelial Neoplasia.

Hematoxylin- and eosin-stained vilVEGF1 and vilVEGF2 jejunal sections show mucosal thickening, cysts, fusion of villi, and increased RBCs compared to WT tissue.

Amelie Boquoi, et al. Gastroenterology. ;136(2):596-606.e4.
2.
Figure 1

Figure 1. Increased red color of vilVEGF2 small intestines. From: Transgenic Expression of VEGF in Intestinal Epithelium Drives Mesenchymal Cell Interactions and Epithelial Neoplasia.

Representative WT (L) and vilVEGF2 (R) intestines. Note the distinct red color and prominent vessels of vilVEGF2 intestines in situ (above) or dissected free.

Amelie Boquoi, et al. Gastroenterology. ;136(2):596-606.e4.
3.
Figure 8

Figure 8. Stimulation of proliferation of APC-mutant human colonocytes by organotypic co-culture with endothelial cells and fibroblasts. From: Transgenic Expression of VEGF in Intestinal Epithelium Drives Mesenchymal Cell Interactions and Epithelial Neoplasia.

(A) Ki67 staining of human APC-mutant colonocytes (‘Epith cells’) co-cultured with colon fibroblasts alone (above) or with MS1 endothelial cells (‘Endo cells’; below) in the matrix. (B) Graph: means ± SD of Ki67 staining of epithelial cells from 4 experiments.

Amelie Boquoi, et al. Gastroenterology. ;136(2):596-606.e4.
4.
Figure 5

Figure 5. Increased proliferation of vilVEGF1 epithelium. From: Transgenic Expression of VEGF in Intestinal Epithelium Drives Mesenchymal Cell Interactions and Epithelial Neoplasia.

Relative lengths of columns of BrdU-labeled epithelial cells in random jejunum and colon sections of WT and vilVEGF1 littermates. Each graph: totals from 28-49 well-oriented microscopic fields of the designated tissue region from 3-5 mice per genotype (x-axis: BrdU column length (arbitrary units), y-axis: number of BrdU columns of a given length).

Amelie Boquoi, et al. Gastroenterology. ;136(2):596-606.e4.
5.
Figure 4

Figure 4. vilVEGF cysts display an inner epithelial lining surrounded by endothelial cells and myofibroblasts. From: Transgenic Expression of VEGF in Intestinal Epithelium Drives Mesenchymal Cell Interactions and Epithelial Neoplasia.

(A, B) Cysts are formed by epithelial cells emerging from crypts. Brown: IHC for Claudin 7. B: dividing (or fusing) cyst. (C-E) Cysts surrounded by CD34-positive cells (D, E; brown), which are largely confined below crypt bases in WT tissue (C). (F) Co-IF staining: α-SMA-positive myofibroblasts (red) are distinct from CD34-positive cells (green; note lack of yellow).

Amelie Boquoi, et al. Gastroenterology. ;136(2):596-606.e4.
6.
Figure 6

Figure 6. Marked stimulation of intestinal neoplasia in vilVEGF1-Min mice. From: Transgenic Expression of VEGF in Intestinal Epithelium Drives Mesenchymal Cell Interactions and Epithelial Neoplasia.

(A) Tumor number in each intestinal section counted under a dissecting microscope from 10 WT-Min mice (L) and 12 vilVEGF1-Min mice (R). (B) Random ‘Swiss roll’ sections of mucosa from 4 WT-Min (L) and 5 vilVEGF1-Min mice (R) scored under a 10× objective for number of macro- (grey bars) and micro-adenomas (black bars; defined as < 3 villi or crypts in width [see inserted images]).

Amelie Boquoi, et al. Gastroenterology. ;136(2):596-606.e4.
7.
Figure 2

Figure 2. Increased VEGF expression in vilVEGF intestines. From: Transgenic Expression of VEGF in Intestinal Epithelium Drives Mesenchymal Cell Interactions and Epithelial Neoplasia.

(A) Relative VEGF mRNA levels assayed by real time RT-PCR in designated whole intestinal segments from 3 WT, 3 vilVEGF1, and 1 vilVEGF2 mice. Column: mean value of mice of designated genotype + standard deviation (each reaction in duplicate, WT colon set to 100 arbitrary units). (B) VEGF levels in recombinant standards or mucosal scrapings (5 μg) from 4 WT, 4 vilVEGF1, and 2 vilVEGF2 mice assayed by ELISA. Column: mean + range of duplicate determinations for one mouse.

Amelie Boquoi, et al. Gastroenterology. ;136(2):596-606.e4.
8.
Figure 7

Figure 7. Advanced histological features in vilVEGF1-Min tumors. From: Transgenic Expression of VEGF in Intestinal Epithelium Drives Mesenchymal Cell Interactions and Epithelial Neoplasia.

(A) Tumor (Tu) with area of undifferentiated cells, characterized by loss of growth in sheets (left of solid line). Right: non-tumor cells. Below dashed line: more differentiated tumor cells. (B) Desmoplastic tumor. Note dense fibrosis and wide separation of neoplastic epithelial sheets. (C) E-cadherin staining is reduced in tumor areas with loss of sheet-like growth (above dashed line). (D) A single villous filled with an adenoma and cyst. Brown: Ki67 staining. (E) Portion of a polycystic mass encompassing more than 100 cysts. Brown: Ki67 staining. (F) vWF staining reveals increased vessels in submucosa (arrows) but not tumor. Arrowheads: scattered vWF-positive cells in tumors.

Amelie Boquoi, et al. Gastroenterology. ;136(2):596-606.e4.

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