TRPM4 Regulates Calcium Oscillations after T Cell Activation

TRPM4 has recently been described as a calcium-activated nonselective (CAN) cation channel that mediates membrane depolarization. However, the functional importance of TRPM4 in the context of calcium (Ca2+) signaling and its effect on cellular responses are not known. Here, the molecular inhibition...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 2004-11, Vol.306 (5700), p.1374-1377
Main Authors: Launay, Pierre, Cheng, Henrique, Srivatsan, Subhashini, Penner, Reinhold, Fleig, Andrea, Kinet, Jean-Pierre
Format: Article
Language:English
Subjects:
Amino acids
Animals
Antibodies
Biological and medical sciences
Blotting, Western
Calcium
Calcium - metabolism
Calcium binding proteins
Calcium Channels - immunology
Calcium Channels - metabolism
Calcium Signaling
Cation Transport Proteins - immunology
Cation Transport Proteins - metabolism
Cations
Cell Line
Cell Line, Tumor
Cell lines
Cell membranes
Cell regulation
Cellular control mechanisms
Depolarization
Fundamental and applied biological sciences. Psychology
HEK293 cells
Humans
Immunoprecipitation
Interleukin-2 - metabolism
Jurkat Cells
Literary Devices
Lymphocyte Activation
Lymphocytes
Membrane Potentials
Mice
Molecular and cellular biology
Patch-Clamp Techniques
Phytohemagglutinins - pharmacology
RNA Interference
Small interfering RNA
Sodium - metabolism
T cell receptors
T cells
T lymphocytes
T-Lymphocytes - immunology
T-Lymphocytes - metabolism
TRPM Cation Channels
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Summary:TRPM4 has recently been described as a calcium-activated nonselective (CAN) cation channel that mediates membrane depolarization. However, the functional importance of TRPM4 in the context of calcium (Ca2+) signaling and its effect on cellular responses are not known. Here, the molecular inhibition of endogenous TRPM4 in T cells was shown to suppress TRPM4 currents, with a profound influence on receptor-mediated Ca2+mobilization. Agonist-mediated oscillations in intracellular Ca2+concentration ([Ca2+]i), which are driven by store-operated Ca2+influx, were transformed into a sustained elevation in [Ca2+]i. This increase in Ca2+influx enhanced interleukin-2 production. Thus, TRPM4-mediated depolarization modulates Ca2+oscillations, with downstream effects on cytokine production in T lymphocytes.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.1098845