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. Author manuscript; available in PMC: 2018 Jul 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2017 May 4;37(7):1380–1390. doi: 10.1161/ATVBAHA.117.309180

Figure 2. Endothelial Mef2c deletion leads to MLC phosphorylation and actin stress-fiber formation in the thoracic aorta.

Figure 2

En face preparation and immunostaining were performed on the thoracic aorta as described in methods. A, B, thoracic aortas from Mef2cTie2EKO and control Mef2cWT mice were immunostained for PECAM-1, F-actin (phalloidin), and nuclei (DAPI). B, Mef2cCdh5EKO (14-days post tamoxifen) and vehicle control were immunostained for VE-Cadherin, F-actin (phalloidin) and nuclei (DAPI); C, thoracic aortas from Mef2cTie2EKO and Mef2cWT control were immunostained for VE-Cadherin, p-MLC, and F-actin (phalloidin). Representative confocal images are shown (n=4).