Transcriptional profiling of regenerating embryonic mouse hearts

Genomics Data
Manuela MagarinJörg-Detlef Drenckhahn

Abstract

The postnatal mammalian heart is considered a terminally differentiated organ unable to efficiently regenerate after injury. In contrast, we have recently shown a remarkable regenerative capacity of the prenatal heart using myocardial tissue mosaicism for mitochondrial dysfunction in mice. This model is based on inactivation of the X-linked gene encoding holocytochrome c synthase (Hccs) specifically in the developing heart. Loss of HCCS activity results in respiratory chain dysfunction, disturbed cardiomyocyte differentiation and reduced cell cycle activity. The Hccs gene is subjected to X chromosome inactivation, such that in females heterozygous for the heart conditional Hccs knockout approximately 50% of cardiac cells keep the defective X chromosome active and develop mitochondrial dysfunction while the other 50% remain healthy. During heart development the contribution of HCCS deficient cells to the cardiac tissue decreases from 50% at mid-gestation to 10% at birth. This regeneration of the prenatal heart is mediated by increased proliferation of the healthy cardiac cell population, which compensates for the defective cells allowing the formation of a fully functional heart by birth. Here we performed microarray RNA express...Continue Reading

References

May 23, 2015·Circulation·Anthony C SturzuSean M Wu
Apr 24, 2016·Journal of Molecular and Cellular Cardiology·Manuela MagarinJörg-Detlef Drenckhahn

Methods Mentioned

BETA
PCR
in vitro transcription
fluorescence activated cell sorting

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