Balancing functions of annexin A6 maintain equilibrium between hypertrophy and apoptosis in cardiomyocytes

Cell Death & Disease
Priyam BanerjeeArun Bandyopadhyay

Abstract

Pathological cardiac hypertrophy is a major risk factor associated with heart failure, a state concomitant with increased cell death. However, the mechanism governing progression of hypertrophy to apoptosis at the single-cell level remains elusive. Here, we demonstrate annexin A6 (Anxa6), a calcium (Ca(2+))-dependent phospholipid-binding protein critically regulates the transition of chronic hypertrophied cardiomyocytes to apoptosis. Treatment of the H9c2(2-1) cardiomyocytes with hypertrophic agonists upregulates and relocalizes Anxa6 with increased cytosolic punctate appearance. Live cell imaging revealed that chronic exposure to hypertrophic agonists such as phenylephrine (PE) compromises the mitochondrial membrane potential (ΔΨm) and morphological dynamics. Such chronic hypertrophic induction also activated the caspases 9 and 3 and induced cleavage of the poly-(ADP-ribose) polymerase 1 (Parp1), which are the typical downstream events in the mitochondrial pathways of apoptosis. An increased rate of apoptosis was evident in the hypertrophied cardiomyocytes after 48-72 h of treatment with the hypertrophic agonists. Anxa6 was progressively associated with the mitochondrial fraction under chronic hypertrophic stimulation, and Anx...Continue Reading

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Citations

Jun 21, 2018·Science Signaling·Ramin RaoufJohn N Wood
Apr 4, 2020·Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism·Sinisa CikicDavid W Busija
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Sep 27, 2018·Molecular and Cellular Biochemistry·Chian Ju JongMorris Karmazyn

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Methods Mentioned

BETA
Fluorescence recovery after photobleaching
co-IP

Software Mentioned

Prism
GraphPad
Adobe Illustrator
ImageJ

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