We are analyzing https://link.springer.com/article/10.1007/s00424-013-1219-y.

Title:
TRPM2 contributes to antigen-stimulated Ca2+ influx in mucosal mast cells | Pflügers Archiv - European Journal of Physiology
Description:
Food allergy (FA) is a common allergic disease without any currently available effective drug therapies. Mucosal mast cells (MMCs) play a particularly important role in FA, and the increase in their cytosolic Ca2+ concentration ([Ca2+]cyt) is considered to be a principal component of the degranulation process. However, the mechanisms governing Ca2+ influx remain poorly understood in MMCs. Recent reports have highlighted the functions of the transient receptor potential melastatin 2 (TRPM2) channel in immunocytes, including its role in monocyte chemokine production and macrophage phagocytic activity. Although TRPM2 gene expression has been demonstrated in mast cells, the significance of such expression remains virtually unknown. In this study, we found that antigen-stimulated degranulation was significantly reduced in mucosal-type bone marrow-derived mast cells (mBMMCs) prepared from TRPM2-knockout (TRPM2-KO) mice (TRPM2-KO mBMMCs) and was suppressed following the administration of three TRPM2 inhibitors with different chemical structures, including econazole, flufenamic acid (FFA), and 2-aminoethoxydiphenyl borate. Furthermore, the antigen-stimulated increase in [Ca2+]cyt was significantly decreased in TRPM2-KO mBMMCs and was also suppressed by the TRPM2 inhibitors econazole and FFA. In addition, thapsigargin-induced increase in [Ca2+]cyt was significantly decreased in TRPM2-KO mBMMCs. These results suggest that TRPM2 may participate in antigen-induced extracellular Ca2+ influx and subsequent degranulation. In addition, TRPM2 inhibitors were shown to improve food allergic reactions in a mouse model. Together, these results suggest that TRPM2 inhibitors suppress MMC degranulation via regulation of the increase in [Ca2+]cyt. Thus, TRPM2 may play a key role in degranulation by modulating intracellular Ca2+ in MMCs.
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article, google, scholar, pubmed, cas, mast, trpm, cells, cell, calcium, kadowaki, allergy, influx, tominaga, degranulation, channels, channel, mucosal, wang, food, role, expression, access, yamamoto, regulation, physiol, activation, immunol, mori, privacy, cookies, content, journal, research, makoto, transient, receptor, potential, kageyamayahara, japan, including, publish, search, antigenstimulated, january, oda, uchida, increase, cacyt, mbmmcs,

Topics {✒️}

protein-coupled receptor-x2/b2 antagonists transient-receptor-potential channel trpv2 month download article/chapter b-cell-receptor stimulation antigen-stimulated ca2+ influx mast-cell degranulation induced lysosomal ca2+-release channel integrated signalling pathways noncapacitative ca2+-entry pathway cyclic adp-ribose redox signal-mediated sensitization related subjects mucosal mast cells ige-induced degranulation monocyte chemokine production endogenous trpm2 channels full article pdf calcium signalling human mast cells mast cell subpopulations modulating intracellular ca2+ mast-cell activation mast cell activation trpm4-mediated control european economic area privacy choices/manage cookies antigen-stimulated degranulation multifunctional ion channel common allergic disease reactive oxygen species calcium influx trpm4 channels cytosolic ca2+ concentration thapsigargin-induced increase ameliorate food allergies antigen-stimulated increase article oda macrophage phagocytic activity ph-dependent antagonist sphingosine kinase-1-dependent intracellular calcium trpm2 channels trpm2 gene expression check access instant access mast cells effective drug therapies mahaut-smith mp antifungal agents clotrimazole nicotinic acetylcholine receptors

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         description:Food allergy (FA) is a common allergic disease without any currently available effective drug therapies. Mucosal mast cells (MMCs) play a particularly important role in FA, and the increase in their cytosolic Ca2+ concentration ([Ca2+]cyt) is considered to be a principal component of the degranulation process. However, the mechanisms governing Ca2+ influx remain poorly understood in MMCs. Recent reports have highlighted the functions of the transient receptor potential melastatin 2 (TRPM2) channel in immunocytes, including its role in monocyte chemokine production and macrophage phagocytic activity. Although TRPM2 gene expression has been demonstrated in mast cells, the significance of such expression remains virtually unknown. In this study, we found that antigen-stimulated degranulation was significantly reduced in mucosal-type bone marrow-derived mast cells (mBMMCs) prepared from TRPM2-knockout (TRPM2-KO) mice (TRPM2-KO mBMMCs) and was suppressed following the administration of three TRPM2 inhibitors with different chemical structures, including econazole, flufenamic acid (FFA), and 2-aminoethoxydiphenyl borate. Furthermore, the antigen-stimulated increase in [Ca2+]cyt was significantly decreased in TRPM2-KO mBMMCs and was also suppressed by the TRPM2 inhibitors econazole and FFA. In addition, thapsigargin-induced increase in [Ca2+]cyt was significantly decreased in TRPM2-KO mBMMCs. These results suggest that TRPM2 may participate in antigen-induced extracellular Ca2+ influx and subsequent degranulation. In addition, TRPM2 inhibitors were shown to improve food allergic reactions in a mouse model. Together, these results suggest that TRPM2 inhibitors suppress MMC degranulation via regulation of the increase in [Ca2+]cyt. Thus, TRPM2 may play a key role in degranulation by modulating intracellular Ca2+ in MMCs.
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         Receptors
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