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. 2016 Mar 3;2016:7631085. doi: 10.1155/2016/7631085

Figure 1.

Figure 1

Increased cardiac vessel density upon Tie2-Cre-mediated conditional PPARβ/δ overexpression. (a) PPARβ/δ immunostaining from heart sections of Tie2-CreERT2; PPARβ/δ + vehicle and Tie2-CreERT2;PPARβ/δ + Tamoxifen animals indicates higher expression levels in the endothelium of Tie2-CreERT2;PPARβ/δ + Tamoxifen animals. Arrows mark PPARβ/δ positive endothelial cells. (b) Quantitative real-time PCRs for PPARβ/δ and Calcineurin in cardiac endothelial cells from Tie2-CreERT2;PPARβ/δ + vehicle and Tie2-CreERT2;PPARβ/δ + Tamoxifen animals (n = 5 for each group). (c) Expression levels for PPARβ/δ, Pecam-1, and eNOS determined by quantitative real-time PCRs from whole mouse heart RNA preparations for both groups (n = 5 for each group). (d) Pecam-1-immunostaining in mouse heart sections and quantification of Pecam-1 signal area density (Tie2-CreERT2;PPARβ/δ + Tamoxifen, n = 5, Tie2-CreERT2;PPARβ/δ + vehicle, n = 5, and Tie2-CreERT2 + Tamoxifen, n = 5). (e) Quantification of Pecam-1 signal area densities and Pecam-1-immunostainings in mouse kidney (upper panel) and pancreas (lower panel) sections (Tie2-CreERT2;PPARβ/δ + Tamoxifen, n = 3, and Tie2-CreERT2;PPARβ/δ + vehicle, n = 3). Scale bars indicate 50 μm. Data are means ± SEM. ∗∗ p < 0.01 and ∗∗∗ p < 0.001.