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. 2018 Dec 10;39:69–82. doi: 10.1016/j.ebiom.2018.12.001

Fig. 1.

Fig. 1

Endothelial cell-enriched AZIN2-sv inhibits HUVEC migration in vitro.

(A) Representative image of in situ hybridization to confirm AZIN2-sv localization in the human heart (bars, 500 μm). Arrows indicate vessels. (B) Representative image of RNA FISH and immunofluorescence for AZIN2-sv and cTnT in the rat heart (bars, 40 μm). Red indicates the location of AZIN2-sv, green indicates the cardiomyocytes, and blue indicates the nucleus. Arrows indicate vessels. (C) AZIN2-sv expression in HCFBs, HUVECs and AC16 cells by qRT-PCR. ⁎p < .05 vs. HCFB; n = 6 per group. (D) Cell migration was assessed using wound-healing assays. Images were captured at 0, 6, 24, and 48 h after TNF-α treatment (10 ng/mL). The horizontal line indicates the wound edge. Migration was estimated by measuring cell numbers within the wounded region (bars, 500 μm). (E) Quantification of the endothelial cell migration rate. ⁎p < .05 vs. control. #p < .05 vs. TNF-a; n = 6 per group. (F) HUVEC invasion assessed by transwell assay (bars, 500 μm). (G) Quantification of invaded cells. ⁎p < .05 vs. control. #p < .05 vs. VEGF; n = 6 per group.