TRPV1 Channels Are New Players in the Reticulum–Mitochondria Ca2+ Coupling in a Rat Cardiomyoblast Cell Line - Hospices Civils de Lyon Accéder directement au contenu
Article Dans Une Revue Cells Année : 2023

TRPV1 Channels Are New Players in the Reticulum–Mitochondria Ca2+ Coupling in a Rat Cardiomyoblast Cell Line

Résumé

The Ca2+ release in microdomains formed by intercompartmental contacts, such as mitochondria-associated endoplasmic reticulum membranes (MAMs), encodes a signal that contributes to Ca2+ 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 Ca2+-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 Ca2+ imaging in four cellular compartments: the endoplasmic reticulum (ER), cytoplasm, mitochondrial matrix, and mitochondrial surface. Our results showed that the ER Ca2+ 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 Ca2+ 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 Ca2+ exchanges.
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hal-04244641 , version 1 (16-10-2023)

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Nolwenn Tessier, Mallory Ducrozet, Maya Dia, Sally Badawi, Christophe Chouabe, et al.. TRPV1 Channels Are New Players in the Reticulum–Mitochondria Ca2+ Coupling in a Rat Cardiomyoblast Cell Line. Cells, 2023, 12 (18), pp.2322. ⟨10.3390/cells12182322⟩. ⟨hal-04244641⟩
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