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. Author manuscript; available in PMC: 2020 Apr 1.
Published in final edited form as: Trends Pharmacol Sci. 2019 Feb 28;40(4):253–266. doi: 10.1016/j.tips.2019.02.004

Figure 2, Key figure. Role of MSTFs in regulating endothelial phenotype.

Figure 2, Key figure.

A. Image showing the focal distribution of lesions in a mouse model of atherosclerosis. The lesions preferentially develop at regions with disturbed flow (DF), such as branches and bends of the blood vessel (indicated by white arrow), but much less in regions of unidirectional laminar flow (UF), such as the straight part of the blood vessel (unpublished data). Note: color saturation of the image is enhanced for presentation purposes.

B. Major MSTFs that are regulated by UF and DF in ECs. The downregulation in shown by blue arrows and upregulation is shown by red arrows.

C. The genes that are regulated by each of the MSTFs in DF and UF treated endothelial cells, are shown.

D. Flow-dependent endothelial gene expression regulates EC phenotype. DF treated endothelial cells show a pro-inflammatory, pro-oxidant, pro-proliferative response, and enhanced endothelial to mesenchymal transition (EndoMT) phenotype. By doing so, DF causes endothelial cell activation and ensuing dysfunction. In contrast, UF treated ECs show anti-inflammatory, anti-oxidant, and anti-proliferative phenotype along with reduced EndoMT and glycolysis, leading to endothelial cell quiescence and vascular homeostasis.