Research Paper Volume 13, Issue 2 pp 2553—2574

TLR2 regulates angiotensin II-induced vascular remodeling and EndMT through NF-κB signaling

Blockade of TLR2 signaling does not affect downstream processes of inflammatory factors and EndMT. (A–C) HUVECs were transfected TLR2 or negative control siRNA. Cells were then exposed to 10 μM Ang II for 6h. mRNA levels of proinflammatory factors were detected [data normalized to β-actin]. (D) Schematic illustration of the experimental model to test the role of Ang II-induced paracrine factors in EndMT. Conditioned media was collected from cells challenged with 10 μM Ang II for 24 h. Media was then added to HUVECs transfected with TLR2 or negative control siRNA. (E) Levels of TLR2 and EndMT-associated proteins were determined in cells treated in panel D. GAPDH was used as loading control. [n = 3; Data shown as Mean ± SEM; **p

Figure 5. Blockade of TLR2 signaling does not affect downstream processes of inflammatory factors and EndMT. (AC) HUVECs were transfected TLR2 or negative control siRNA. Cells were then exposed to 10 μM Ang II for 6h. mRNA levels of proinflammatory factors were detected [data normalized to β-actin]. (D) Schematic illustration of the experimental model to test the role of Ang II-induced paracrine factors in EndMT. Conditioned media was collected from cells challenged with 10 μM Ang II for 24 h. Media was then added to HUVECs transfected with TLR2 or negative control siRNA. (E) Levels of TLR2 and EndMT-associated proteins were determined in cells treated in panel D. GAPDH was used as loading control. [n = 3; Data shown as Mean ± SEM; **p<0.01 compared to negative control; #p<0.05 and ##p<0.01 compared to Ang II exposed negative control].