Skip to main content
. Author manuscript; available in PMC: 2015 Nov 6.
Published in final edited form as: Cell Stem Cell. 2014 Nov 6;15(5):589–604. doi: 10.1016/j.stem.2014.10.003

Figure 3. Heart regeneration is controlled by miR-99/100.

Figure 3

(A–C) Following adult zebrafish heart amputation, exogenous intra-cardiac administration of 0.2 μg miR-99/100 mimics every second day for a total of 14 days led to defective cardiac regeneration in amputated zebrafish (A, upper row), as determined by reduced BrdU incorporation (A, lower row and C). (D–F) miR-99/100 antagomiRs exerted the opposite effect in uninjured adult animals, inducing a significant increase in ventricle size (D, upper panels and E) and increasing cardiomyocyte proliferation in the absence of heart damage (D, lower panels and F). (G–I) Chemical inhibition of fnt activity with tipifarnib upon intraperitoneal injection (final concentration 0.02 mg/animal) every 2 days for 14 days dramatically reduced heart regeneration in amputated zebrafish as compared to control animals administered with the solvent DMSO control (G and H) and reducing cardiomyocyte proliferation as assessed by BrdU incorporation (G, lower panels and I). Dashed line: amputation plane. Boxed area: magnified detail. Data are represented as mean ± s.e.m. *p<0.05. n = 6 animals, three different sections per animal were used for quantitative analyses.