FIGURE

Fig. 4

ID

ZDB-FIG-170519-29

Publication

Benz et al., 2016 - miR-19b Regulates Ventricular Action Potential Duration in Zebrafish

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Fig. 4

Loss of miR-19b induces prolongation of the action potential

(a) Schematic illustration of an action potential with major depolarizing and repolarizing currents depicted. Terfenadine inhibits I_Kr current, thereby prolonging the ventricular action potential. (b) Atrial and ventricular m-mode recorded from control and MO19b-injected Tg(Myl7:GFP) zebrafish embryos after 30 μM Terfenadine treatment. (b,c) 25% ± 4.1% of miR-19b deficient embryos develop an AV-Block with the ventricle skipping every other contraction, whereas control injected embryos show no phenotype. (±sd; n = 3 with ≥10 animals per group; p < 0.05) (d,e) Patch-clamp Experiments revealed that morpholino-mediated loss of miR-19b results in prolonged action potentials with up to 57% ± 3.8% and 39% ± 3.5% prolongation of APD₅₀ and APD₉₀, respectively (±sd; n ≥ 10 from 5 hearts; p < 0.05). Additionally, the notch appeared to be less pronounced (stars).

Expression Data

Gene:	EGFP
Fish:	twu34Tg twu34Tg + MO2-dre-mir-19b
Condition:	chemical treatment by environment: Terfenadine
Knockdown Reagent:	MO2-dre-mir-19b
Anatomical Terms:	atrium cardiac ventricle
Stage:	Long-pec

Expression Detail

Antibody Labeling

Phenotype Data

Fish:	WT + MO2-dre-mir-19b twu34Tg + MO2-dre-mir-19b
Condition:	chemical treatment by environment: Terfenadine
Knockdown Reagent:	MO2-dre-mir-19b
Observed In:	cardiac ventricle cardiac muscle contraction cardiac ventricle ventricular cardiac muscle cell action potential
Stage:	Long-pec

Phenotype Detail

Acknowledgments

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