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. 2020 Jan 14;141(8):667–677. doi: 10.1161/CIRCULATIONAHA.119.044582

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© 2020 The Authors.

Circulation is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited.

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Figure 3. — Production of I16 mRNA in Reg1^-/- hearts under pressure overload. Reg1^+/+ and Reg1^−/− hearts 4 weeks (A through D) or 1 week (E) after transverse aortic constriction (TAC) were analyzed. Data were evaluated by the Student t test (C and D) or 1-way analysis of variance with the Bonferroni post hoc test (E). Data are mean ± SEM. ^*P<0.05, ^***P<0.001. A, Double staining of TAC-operated Reg1^−/− heart sections with anti-CD68 (red) and anti-CD11c (green) antibodies. B, Double staining of TAC-operated Reg1^−/− heart sections with anti-CD68 (red) and anti-CD206 (green) antibodies. Scale bar, 100 µm. C, The ratio of CD11c-positive or CD206-positive to CD68-postive cell numbers (n=3). D, In situ hybridization for Il6 mRNA (red) in Reg1^+/+ or Reg1^−/− hearts, followed by immunostaining with α-sarcomeric action antibody (green). Scale bar, 100 µm. Right graph shows the number of red dots in cardiomyocytes. E, Tnfa and Il6 mRNA levels 1 week after TAC. Total n=5 (sham–Reg1^+/+), 5 (TAC–Reg1^+/+), 5 (sham–Reg1^−/−), or 6 (TAC–Reg1^−/−) per group. Gapdh mRNA was used as the loading control. The averaged value in sham-operated Reg1^+/+ mice was set equal to 1.