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. Author manuscript; available in PMC: 2013 Mar 16.
Published in final edited form as: Circ Res. 2012 Feb 16;110(6):818–830. doi: 10.1161/CIRCRESAHA.111.259663

Figure 6. CIP represses cardiomyocyte hypertrophy.

Figure 6

(A) Gene expression of CIP and hypertrophic marker, ANP and BNP, determined by qPCR in heart samples from Sham group and Transverse Aortic Constriction (TAC) group at two different time point (3 days and 7 days). n=4.

(B) Gene expression of CIP and hypertrophic marker ANP determined by qPCR in heart samples from 1 month old Myh6-calcineurin transgenic mice (CnA) and control littermates (WT). n=3.

(C) Western blotting analysis showing decreased expression of CIP proteins in neonatal rat cardiomyocytes, which were induced to develop hypertrophy by different hypertrophic agonists in vitro. None treated sample serves as a control. LIF, leukemia inhibitory factor; ET-1, Endothelin-1; PE, phenylephrine.

(D) Quantitative RT-PCR showing CIP expression in rat neonatal cardiomyocytes with or without phenylephrine (PE) treatment. *P<0.05.

(E) CIP represses PE-induced hypertrophy in neonatal cardiomyocytes. Representative images of cardiomyocytes infected with adenoviral-CIP (ad-CIP) or adenoviral-GFP (ad-GFP) (to serve as controls) and treated with phenylephrine (PE) (or without treatment to serve as controls). Anti α-actinin antibodies were used to mark cardiomyocytes (red). DAPI marks nucleus. Bar = 21 μm.

(F) Quantitative analysis of cardiomyocyte cell size. ~300 cells positive for α-actinin from each treatment were randomly chosen for surface area measurement. *P<0.05.

(G) Quantitative RT-PCR showing the downregulation of PE-induced expression of hypertrophic marker ANP, BNP and β-MHC when CIP was overexpressed in neonatal cardiomyocytes. n=4. *P<0.05. ANP, atrial natriuretic peptide; BNP, brain natriuretic peptide; β-MHC, β-myosin heavy chain.