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. Author manuscript; available in PMC: 2020 Apr 12.
Published in final edited form as: Circ Res. 2019 Apr 12;124(8):1253–1265. doi: 10.1161/CIRCRESAHA.118.314567

Figure 5. SMCs regulate endothelial cell migration through a PKCδ-mediated paracrine mechanism.

Figure 5.

(A&B) Wound closure of endothelial monolayers grown in medium condition by AdNull- or AdPKCδ-infected and TNFα- (1ng/ml) or PMA- (1nM) treated SMCs. ECs were labeled with CMFDA green fluorescence dye for visualization. Dashed lines mark the wound edges generated by scratching. Wound closure was determined by the percentage of the recovered area over the total injured area using ImageJ software. Scale bar = 50 μm. (C) EC migration toward medium condition by AdNull-, or AdPKCδ-infected and PMA- (1nM) treated SMCs. ECs were labeled with CMFDA green fluorescence dye and counterstained with DAPI for visualization. Representative images of migrated cells are shown. Data are expressed as the mean number of migrated cells/fields±SEM. Scale bar = 50 μm. (D&E) Proliferation and viability of endothelial cells grew in medium conditioned by AdNull- and AdPKCδ-infected and PMA- (1nM) treated SMCs were measured by BrdU incorporation and CellTiter-Glo® luminescent cell viability assay, respectively. Results are expressed as mean±SEM. n=3-5, *p<0.05, Two-tailed Student’s t-test.