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. 2021 Mar 25;10:e66079. doi: 10.7554/eLife.66079

Figure 5. Rho A activity is required for cardiogenic responses to mitogens.

(A) Summary of transgenic animals used in Rho A inhibition experiments. (B) Timeline of experiments for Nrg1-overexpression (OE, blue), Vegfaa-OE (red), and alfacalcidol treatment (orange). (C, E, G) Immunofluorescence images of ventricles stained for Mef2/EdU from animals overexpressing Nrg1 (C) or Vegfaa (E) in cardiomyocytes, or injected with alfacalcidol (G). Hearts were treated with either vehicle or Rhosin. Scale bar, 50 μm. (D, F, H) Inhibition of Rho A by Rhosin reduces cardiomyocyte (CM) proliferation. Quantification of Mef2/EdU staining. Five to six animals were assessed for each group in two independent experiments. Data show mean ± SEM (Mann–Whitney U test).

Figure 5.

Figure 5—figure supplement 1. Rho A levels in hearts of cardiac mitogen-treated animals.

Figure 5—figure supplement 1.

(A) Western blot analysis of Rho A levels in ventricles of zebrafish with Nrg1-overexpression (OE), Vegfaa-OE, or vitamin D receptor activation via alfacalcidol. (B) Quantification of western blot shown in (A). In untreated hearts, Rho A levels were set to 100%. Levels were normalized to loading control GAPDH.