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Dysregulation of c-kit expression parallels the development of spontaneous genetic cardiac hypertrophy

- Marques, Francine, Prestes, Priscilla, Lewandowski, Paul, Harrap, Stephen, Charchar, Fadi

  • Authors: Marques, Francine , Prestes, Priscilla , Lewandowski, Paul , Harrap, Stephen , Charchar, Fadi
  • Date: 2015
  • Type: Text , Conference paper
  • Relation: Cardiac Society of Australia and New Zealand Annual Scientific Meeting and the International Society for Heart Research Australasian Section Annual Scientific Meeting; Melbourne, Victoria, Australia; 13th-16th August 2016; published in Heart, Lung and Circulation. Vol. 24, p. S401-S401
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  • Description: Objective: The molecular processes associated with cardiac hypertrophy independent of blood pressure are still largely unknown. The hypertrophic heart rate (HHR) is normotensive and born with a reduced complement of cardiomyocytes that predisposes to cardiac hypertrophy and failure in later life. We investigated the expression of c-kit gene, a marker of cardiac stem cells and myocardial regeneration that could contribute to hypertrophy. Methods: Left ventricular c-kit mRNA expression was measured by real-time PCR in HHR and control strain in neonatal and 38-week old rats (n=7-12/group). We tested for linkage of c-kit expression with neonatal cardiac size in 197 second generation crosses (F2) of HHR and control strain. Results: c-kit mRNA was slightly up-regulated in neonatal (fold change +1.3, P=0.02) and markedly so in 38-week old HHR (+35.5, P=0.0003). Cardiac weight index was positively correlated with neonatal myocardial c-kit mRNA in the F2 population (r=0.19, P=0.007). Conclusions: In HHR hearts c-kit expression appears increased throughout life, but more so in the adult where cardiac hypertrophy is established and leading to failure. In aged hypertrophic hearts, over-expression of c-kit is likely a compensatory mechanism of the failing heart. Previous studies showed an activation of cardiac stem cells in the hypertrophic myocardium. Our study suggests that c-kit might be involved from an early age in mechanisms that lead to cardiac hypertrophy in adulthood.

MicroRNA-34a and tert act as epi-drivers of cardiac telomere length and polygenic cardiac hypertrophy

- Booth, Scott, Marques, Francine, Prestes, Priscilla, Curl, Claire, Delbridge, Lea, Lewandowski, Paul, Harrap, Stephen, Charchar, Fadi

  • Authors: Booth, Scott , Marques, Francine , Prestes, Priscilla , Curl, Claire , Delbridge, Lea , Lewandowski, Paul , Harrap, Stephen , Charchar, Fadi
  • Date: 2015
  • Type: Text , Journal article
  • Relation: Heart, Lung and Circulation Vol. 24, no. S3 (2015), p. S180-S181
  • Full Text: false
  • Reviewed:
  • Description: Cardiac hypertrophy is one of the main risk factors forheart failure. Here we aimed to investigate whether cardiactelomere length contributes to polygenic cardiac hypertro-phy independent of blood pressure. We also investigatedwhether changes in telomere length were due to the telomereregulators microRNA-34a,Ppp1r10(also known asPnuts)and telomerase. We used the hypertrophic heart rat (HHR),a normotensive model of polygenetic cardiac hypertrophy,and compared it to age-matched controls. Telomere length, microRNA levels, gene expression and telomerase activitywere measured in isolated cardiomyocytes and left ventricletissue using real-time PCR. Telomere length was significantlylonger in 2-day and 38-week-old HHR, but shorter at 4-and 13-week HHR. In the HHR, telomere length becameshorter early in development, while in the control straintelomere shortening was only observed in late adulthood.Telomere length was the main determinant of cardiac mass.
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