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Nakanishi T, Markwald RR, Baldwin HS, et al., editors. Etiology and Morphogenesis of Congenital Heart Disease: From Gene Function and Cellular Interaction to Morphology [Internet]. Tokyo: Springer; 2016. doi: 10.1007/978-4-431-54628-3_11

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Etiology and Morphogenesis of Congenital Heart Disease: From Gene Function and Cellular Interaction to Morphology [Internet].

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Fig. 11.3. Meis1 overexpression limits neonatal heart regeneration following MI.

Fig. 11.3

Meis1 overexpression limits neonatal heart regeneration following MI. (a) Schematic of Meis1 overexpression (OE) in the heart. Control mice were αMHC-tTA, Meis1 (OE) mice were pTREMeis1-αMHC-tTA. (b) qRT–PCR demonstrates overexpression of Meis1. (c) HW-to-BW ratio in control and Meis1 (OE) mice. (d) H & E staining of WT and Meis1 (OE) hearts. (e) LV systolic function quantified by EF. (f) WGA staining and cell size quantification. (g) Immunostaining image showing co-localization of pH3, TnnT2, and Hoechst in Meis1 (OE) heart at P3. Graph shows quantification of pH3+TnnT2+ nuclei. (h) Schematic of neonatal MI during the regenerative window at P1. (i) LV systolic function of WT and Meis1 (OE) hearts at 21 days post-MI. (j) Trichromes at day 21 post-MI. (k) qRT–PCR of CDKIs in hearts of Meis1 (OE) compared to control

From: Chapter 11, Meis1 Regulates Postnatal Cardiomyocyte Cell Cycle Arrest

Copyright 2016, The Author(s)

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