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GDF-11 prevents cardiomyocyte hypertrophy by maintaining the sarcoplasmic reticulum-mitochondria communication

Valeria Garrido-Moreno¹, Alexis Díaz-Vegas¹, Camila López-Crisosto¹

¹Advanced Center for Chronic Diseases (ACCDiS), Faculty of Chemical and Pharmaceutical Sciences & Faculty of Medicine, University of Chile, Santiago, Chile.

Pharmacological Research

|May 17, 2019

Insights

Growth differentiation factor 11 (GDF11) prevents cardiac hypertrophy by maintaining communication between the sarcoplasmic reticulum and mitochondria. This preserves mitochondrial function and energy metabolism, crucial for cardiomyocyte health.

Area of Science:

Cardiovascular Biology
Cellular Metabolism
Mitochondrial Function

Background:

Cardiac hypertrophy is a complex condition with unclear molecular mechanisms.
Norepinephrine (NE) triggers hypertrophy by disrupting sarcoplasmic reticulum (SR)-mitochondria communication and calcium (Ca2+) handling.
Growth differentiation factor 11 (GDF11) has shown potential in preventing cardiac hypertrophy, but its mechanism is not fully understood.

Purpose of the Study:

To investigate the anti-hypertrophic mechanism of GDF11.
To determine if GDF11 prevents the loss of SR-mitochondria communication induced by NE.
To elucidate GDF11's role in regulating cardiomyocyte calcium and mitochondrial metabolism.

Main Methods:

Primary cell culture of neonatal rat ventricular myocytes.
Treatment with norepinephrine (NE) to induce hypertrophy.
Assessment of SR-mitochondria contact sites using microscopy.
Measurement of mitochondrial Ca2+ uptake and oxidative metabolism.

Main Results:

GDF11 prevented NE-induced cardiac hypertrophy in cultured myocytes.
GDF11 attenuated the disruption of SR-mitochondria physical contact sites caused by NE.
GDF11 enhanced mitochondrial Ca2+ uptake and boosted oxidative mitochondrial metabolism.

Conclusions:

GDF11 maintains SR-mitochondria communication, vital for cardiomyocyte Ca2+ transfer and energy production.
Preservation of SR-mitochondria crosstalk by GDF11 is a key mechanism against NE-induced hypertrophy.
GDF11's action on mitochondrial function and calcium handling offers a potential therapeutic strategy for cardiac hypertrophy.

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Abstract:

Growth differentiation factor 11 (GDF11) is a novel factor with controversial effects on cardiac hypertrophy both in vivo and in vitro. Although recent evidence has corroborated that GDF11 prevents the development of cardiac hypertrophy, its molecular mechanism remains unclear. In our previous work, we showed that norepinephrine (NE), a physiological pro-hypertrophic agent, increases cytoplasmic Ca²⁺ levels accompanied by a loss of physical and functional communication between sarcoplasmic reticulum (SR) and mitochondria, with a subsequent reduction in the mitochondrial Ca²⁺ uptake and mitochondrial metabolism. In order to study the anti-hypertrophic mechanism of GDF11, our aim was to investigate whether GDF11 prevents the loss of SR-mitochondria communication triggered by NE. Our results show that: a) GDF11 prevents hypertrophy in cultured neonatal rat ventricular myocytes treated with NE. b) GDF11 attenuates the NE-induced loss of contact sites between both organelles. c) GDF11 increases oxidative mitochondrial metabolism by stimulating mitochondrial Ca²⁺ uptake. In conclusion, the GDF11-dependent maintenance of physical and functional communication between SR and mitochondria is critical to allow Ca²⁺ transfer between both organelles and energy metabolism in the cardiomyocyte and to avoid the activation of Ca²⁺-dependent pro-hypertrophic signaling pathways.

Keywords:

Ca(2+)Cardiomyocyte hypertrophy GDF11 Interorganelle communication Mitochondrial metabolism Norepinephrine Sarcoplasmic reticulum-mitochondria contact sites

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