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Involvement of interaction between TRPM2 and IKCA1 in temperature-dependent movement and IL-1β production in mouse
Aykut Deveci1, Makiko Kashio2, Sandra Derouiche3
1Division of Cell Signaling, National Institute for Physiological Sciences, National Institutes of Natural Sciences, Okazaki 444-8787, Japan; Graduate Institute of Advanced Studies, The Graduate University for Advanced Studies (SOKENDAI), Okazaki 444-8585, Japan.
Abstract:
Transient potential melastatin 2 (TRPM2) plays important roles in Ca2 + signaling in tissues and cells, and contributes to various cellular functions. The Ca2+ influx induced by TRPM2 may activate the intermediate conductance Ca2+-activated potassium channel (IKCA1/ KCa3.1/ SK4) and trigger K+ efflux. Here we demonstrate that a functional interaction between TRPM2 and IKCA1 contributes to cell volume changes in HEK293T cells and mouse primary microglia. Ca2+ entering cells through TRPM2 causes K+ efflux, followed by cell shrinkage upon water efflux. In addition, mouse microglia exhibited temperature-dependent movement in vitro that was modulated by the TRPM2-IKCA1 interaction within the physiological body temperature range. This interaction was also found to be involved in cytokine production in microglia. Understanding how the TRPM2-IKCA1 interaction in microglia can promote cell movement and cytokine production could be valuable for developing new strategies for treatments of diseases involving TRPM2.
Insights
Transient Receptor Potential Melastatin 2 (TRPM2) and intermediate conductance calcium-activated potassium channel 1 (IKCA1) interact to regulate cell volume and microglial function. This TRPM2-IKCA1 interaction influences cell movement and cytokine production in microglia.
Area of Science:
- Ion channel physiology
- Cell signaling
- Neuroimmunology
Background:
- Transient Receptor Potential Melastatin 2 (TRPM2) is crucial for calcium (Ca2+) signaling in various cells and tissues.
- TRPM2-mediated Ca2+ influx can activate intermediate conductance Ca2+-activated potassium channels (IKCA1), leading to potassium (K+) efflux.
Purpose of the Study:
- To investigate the functional interaction between TRPM2 and IKCA1.
- To elucidate the role of this interaction in cell volume regulation and microglial functions, including movement and cytokine production.
Main Methods:
- Experiments were conducted using HEK293T cells and primary mouse microglia.
- Functional assays were used to assess cell volume changes, Ca2+ influx, K+ efflux, and microglial cell movement.
- The involvement of the TRPM2-IKCA1 interaction in cytokine production was evaluated.
Main Results:
- A functional interaction between TRPM2 and IKCA1 was demonstrated, contributing to cell volume changes in HEK293T cells and mouse microglia.
- TRPM2-mediated Ca2+ influx triggers K+ efflux, resulting in cell shrinkage via water efflux.
- The TRPM2-IKCA1 interaction modulates temperature-dependent microglial movement within the physiological temperature range and influences cytokine production.
Conclusions:
- The TRPM2-IKCA1 interaction is a key regulator of cell volume and microglial behavior.
- Understanding this interaction provides insights into microglial responses to temperature and inflammatory stimuli.
- Targeting the TRPM2-IKCA1 pathway may offer novel therapeutic strategies for diseases involving TRPM2 dysfunction.
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