hCLOCK Causes Rho-Kinase-Mediated Endothelial Dysfunction and NF-κB-Mediated Inflammatory Responses

Figure 2

Effect of knockdown of hCLOCK on ROS production, tube formation, and RhoA activity. (a) Western blot analysis was performed to confirm successful knockdown of hCLOCK. (b) Representative images obtained during analysis of fluorescence intensity, comparing ROS levels with and without knockdown of hCLOCK. The control HUVEC group was kept in normoxic conditions and was transduced with a control retroviral vector. The SCR HUVEC group was exposed to hypoxic conditions and was transduced with a scrambled control retroviral vector. The shCLOCK HUVEC group was exposed to hypoxic conditions and transduced with an hCLOCK knockdown retroviral vector. Bar graph shows relative ROS levels normalized to the normoxic control group. compared to control; compared to SCR. (c) Photographs obtained during tube-formation assay comparing tube-formation levels in HUVECs with and without knockdown of hCLOCK. Bar graph quantifies relative tube-formation levels. compared to control; compared to SCR. (d) Western blot analysis showing activated RhoA normalized to total RhoA in HUVECs with and without knockdown of hCLOCK.

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