TRPV1 Channels Are New Players in the Reticulum–Mitochondria Ca[sup.2+] Coupling in a Rat Cardiomyoblast Cell Line

• Published in: Cells (Basel, Switzerland) Vol. 12; no. 18
• Main Authors: Tessier, Nolwenn, Ducrozet, Mallory, Dia, Maya, Badawi, Sally, Chouabe, Christophe, Crola Da Silva, Claire, Ovize, Michel, Bidaux, Gabriel, Van Coppenolle, Fabien, Ducreux, Sylvie
• Format: Journal Article
• Language: English
• Published: MDPI AG 01.09.2023
• Subjects: Cell receptors; Endoplasmic reticulum; Health aspects; Mitochondria; Stem cells; France
• ISSN: 2073-4409; 2073-4409
• DOI: 10.3390/cells12182322

The Ca[sup.2+] release in microdomains formed by intercompartmental contacts, such as mitochondria-associated endoplasmic reticulum membranes (MAMs), encodes a signal that contributes to Ca[sup.2+] homeostasis and cell fate control. However, the composition and function of MAMs remain to be fully defined. Here, we focused on the transient receptor potential vanilloid 1 (TRPV1), a Ca[sup.2+] -permeable ion channel and a polymodal nociceptor. We found TRPV1 channels in the reticular membrane, including some at MAMs, in a rat cardiomyoblast cell line (SV40-transformed H9c2) by Western blotting, immunostaining, cell fractionation, and proximity ligation assay. We used chemical and genetic probes to perform Ca[sup.2+] imaging in four cellular compartments: the endoplasmic reticulum (ER), cytoplasm, mitochondrial matrix, and mitochondrial surface. Our results showed that the ER Ca[sup.2+] released through TRPV1 channels is detected at the mitochondrial outer membrane and transferred to the mitochondria. Finally, we observed that prolonged TRPV1 modulation for 30 min alters the intracellular Ca[sup.2+] equilibrium and influences the MAM structure or the hypoxia/reoxygenation-induced cell death. Thus, our study provides the first evidence that TRPV1 channels contribute to MAM Ca[sup.2+] exchanges.