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Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors
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The ABA/LANCL1-2 Hormone/Receptors System Controls ROS Production in Cardiomyocytes through ERRα
Sonia Spinelli1, Lucrezia Guida2, Mario Passalacqua2
1Laboratory of Molecular Nephrology, IRCCS Istituto Giannina Gaslini, Via Gerolamo Gaslini 5, 16147 Genova, Italy.
Biomedicines
|September 28, 2024
Summary
The abscisic acid (ABA) hormone system, via LANCL1-2 receptors, improves heart cell mitochondrial function and resilience. This ABA/LANCL system controls reactive oxygen species (ROS) turnover in H9c2 cells through ERRα.
Area of Science:
- Cardiology
- Molecular Biology
- Cellular Physiology
Background:
- Abscisic acid (ABA) hormone receptors LANCL1 and LANCL2 are implicated in cardiomyocyte mitochondrial function.
- Overexpression of LANCL1/2 in H9c2 cells enhances mitochondrial proton gradient, respiration, and vitality post-hypoxia/reoxygenation.
Purpose of the Study:
- To investigate the role of the ABA/LANCL1-2 system in regulating reactive oxygen species (ROS) turnover in H9c2 cells.
- To determine the involvement of the transcription factor ERRα in the ABA/LANCL1-2 mediated control of ROS.
Main Methods:
- H9c2 cells were genetically modified for LANCL1/2 overexpression or silencing, with or without ERRα knockdown.
- Quantitative real-time PCR (qRT-PCR) and Western blot analyzed enzymes of radical production/scavenging.
- Fluorescent probes measured mitochondrial proton gradient and ROS levels.
Main Results:
- LANCL1/2 overexpression decreased ROS-generating enzymes, increased ROS-scavenging enzymes, and reduced mitochondrial ROS.
- LANCL1/2 silencing produced opposite effects on ROS turnover.
- ERRα knockdown abolished the beneficial effects of LANCL1/2 overexpression on ROS metabolism.
Conclusions:
- The ABA/LANCL1-2 system modulates ROS turnover in H9c2 cardiomyocytes via the transcription factor ERRα.
- The ABA/LANCL system represents a potential therapeutic target for enhancing cardiomyocyte mitochondrial health and oxidative stress resilience.
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