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. 2015 Oct 1;37(18):1469–1475. doi: 10.1093/eurheartj/ehv449

Figure 4.

Figure 4

Irx3 mutations were less effective in up-regulation of Cx40 and Scn5a. (A) Homology of human IRX3 and murine Irx3. Amino acids conserved between human IRX3 and mouse Irx3 are shown by white letters in black box. Two missense mutation sites found in ventricular fibrillation patients in this study are shown by reverse triangles. (B and C) Effects of adenoviral infection with Irx3 into HL-1 cells on the expression of Cx40 (B) and Scn5a (C). The expression of Cx40 and Scn5a was normalized to that of Irx3. Adenoviral infection with wild-type Irx3 increased the expression of Cx40 and Scn5a. Up-regulation of Cx40 and Scn5a was significantly less in R426P (n = 6) and P491T (n = 6) infection than in wild-type Irx3 infection (n = 6). The data are presented actual plots beside the box whisker plot in these and following figures. (D and E) Effects of adenoviral infection with Irx3 into neonatal murine ventricular myocytes on the expression of Cx40 (D) and Scn5a (E). The expression of Cx40 and Scn5a was normalized to that of Irx3. Adenoviral infection with wild-type Irx3 into neonatal murine ventricular myocytes increased the expression of Cx40 and Scn5a. Up-regulation of Cx40 and Scn5a was significantly less in R426P (n = 6) and P491T (n = 6) infection than in wild-type Irx3 infection (n = 6). (F and G) Effects of transfection of HL-1 cells with Irx3 in pcDNA3 vector on the expression of Cx40 (F) and Scn5a (G). The expression of Cx40 and Scn5a was normalized to that of Irx3. Transfection of HL-1 cells with wild-type Irx3 increased the expression of Cx40 and Scn5a. Up-regulation of Cx40 and Scn5a was significantly less in R426P (n = 6) and P491T (n = 6) infection than in wild-type Irx3 transfection (n = 6).