TRPM4 regulates migration of mast cells in mice

Takahiro Shimizu; Grzegorz Owsianik; Marc Freichel; Veit Flockerzi; Bernd Nilius; Rudi Vennekens

doi:10.1016/j.ceca.2008.10.005

TRPM4 regulates migration of mast cells in mice

Takahiro Shimizu, Grzegorz Owsianik, Marc Freichel, Veit Flockerzi, Bernd Nilius^*, Rudi Vennekens

^*この論文の責任著者

薬物生理学研究室

研究成果: ジャーナルへの寄稿 › 学術論文 › 査読

86 被引用数 (Scopus)

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We demonstrate here that the transient receptor potential melastatin subfamily channel, TRPM4, controls migration of bone marrow-derived mast cells (BMMCs), triggered by dinitrophenylated human serum albumin (DNP-HSA) or stem cell factor (SCF). Wild-type BMMCs migrate after stimulation with DNP-HSA or SCF whereas both stimuli do not induce migration in BMMCs derived from TRPM4 knockout mice (trpm4^-/-). Mast cell migration is a Ca²⁺-dependent process, and TRPM4 likely controls this process by setting the intracellular Ca²⁺ level upon cell stimulation. Cell migration depends on filamentous actin (F-actin) rearrangement, since pretreatment with cytochalasin B, an inhibitor of F-actin formation, prevented both DNP-HSA- and SCF-induced migration in wild-type BMMC. Immunocytochemical experiments using fluorescence-conjugated phalloidin demonstrate a reduced level of F-actin formation in DNP-HSA-stimulated BMMCs from trpm4^-/- mice. Thus, our results suggest that TRPM4 is critically involved in migration of BMMCs by regulation of Ca²⁺-dependent actin cytoskeleton rearrangements.

本文言語	英語
ページ（範囲）	226-232
ページ数	7
ジャーナル	Cell Calcium
巻	45
号	3
DOI	https://doi.org/10.1016/j.ceca.2008.10.005
出版ステータス	出版済み - 2009/03

ASJC Scopus 主題領域

生理学
分子生物学
細胞生物学

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10.1016/j.ceca.2008.10.005

引用スタイル

@article{8a61820b7a954117aa22eccdc1c21231,

title = "TRPM4 regulates migration of mast cells in mice",

abstract = "We demonstrate here that the transient receptor potential melastatin subfamily channel, TRPM4, controls migration of bone marrow-derived mast cells (BMMCs), triggered by dinitrophenylated human serum albumin (DNP-HSA) or stem cell factor (SCF). Wild-type BMMCs migrate after stimulation with DNP-HSA or SCF whereas both stimuli do not induce migration in BMMCs derived from TRPM4 knockout mice (trpm4-/-). Mast cell migration is a Ca2+-dependent process, and TRPM4 likely controls this process by setting the intracellular Ca2+ level upon cell stimulation. Cell migration depends on filamentous actin (F-actin) rearrangement, since pretreatment with cytochalasin B, an inhibitor of F-actin formation, prevented both DNP-HSA- and SCF-induced migration in wild-type BMMC. Immunocytochemical experiments using fluorescence-conjugated phalloidin demonstrate a reduced level of F-actin formation in DNP-HSA-stimulated BMMCs from trpm4-/- mice. Thus, our results suggest that TRPM4 is critically involved in migration of BMMCs by regulation of Ca2+-dependent actin cytoskeleton rearrangements.",

keywords = "Actin cytoskeleton, Antigen, Mast cells, Migration, TRP channel, TRPM4, Transgenic mice",

author = "Takahiro Shimizu and Grzegorz Owsianik and Marc Freichel and Veit Flockerzi and Bernd Nilius and Rudi Vennekens",

note = "Funding Information: We thank all members of the Leuven laboratory for helpful suggestions and criticisms and S. Buchholz and M. Benoit for the help with BMMC culture. This work was supported by grants from the Interuniversity Attraction Poles Programme – Belgian State – Belgian Science Policy, P6/28, and the Flemish Government (Excellentiefinanciering EF/95/010), and the Uehara memorial foundation and the Deutsche Forschingsgemeinschaft (MF, VF), Forschungsausschuss Universit{\"a}t des Saarlandes and the HOMFOR program (MF, VF).",

year = "2009",

month = mar,

doi = "10.1016/j.ceca.2008.10.005",

language = "英語",

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pages = "226--232",

journal = "Cell Calcium",

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T1 - TRPM4 regulates migration of mast cells in mice

AU - Shimizu, Takahiro

AU - Owsianik, Grzegorz

AU - Freichel, Marc

AU - Flockerzi, Veit

AU - Nilius, Bernd

AU - Vennekens, Rudi

N1 - Funding Information: We thank all members of the Leuven laboratory for helpful suggestions and criticisms and S. Buchholz and M. Benoit for the help with BMMC culture. This work was supported by grants from the Interuniversity Attraction Poles Programme – Belgian State – Belgian Science Policy, P6/28, and the Flemish Government (Excellentiefinanciering EF/95/010), and the Uehara memorial foundation and the Deutsche Forschingsgemeinschaft (MF, VF), Forschungsausschuss Universität des Saarlandes and the HOMFOR program (MF, VF).

PY - 2009/3

Y1 - 2009/3

N2 - We demonstrate here that the transient receptor potential melastatin subfamily channel, TRPM4, controls migration of bone marrow-derived mast cells (BMMCs), triggered by dinitrophenylated human serum albumin (DNP-HSA) or stem cell factor (SCF). Wild-type BMMCs migrate after stimulation with DNP-HSA or SCF whereas both stimuli do not induce migration in BMMCs derived from TRPM4 knockout mice (trpm4-/-). Mast cell migration is a Ca2+-dependent process, and TRPM4 likely controls this process by setting the intracellular Ca2+ level upon cell stimulation. Cell migration depends on filamentous actin (F-actin) rearrangement, since pretreatment with cytochalasin B, an inhibitor of F-actin formation, prevented both DNP-HSA- and SCF-induced migration in wild-type BMMC. Immunocytochemical experiments using fluorescence-conjugated phalloidin demonstrate a reduced level of F-actin formation in DNP-HSA-stimulated BMMCs from trpm4-/- mice. Thus, our results suggest that TRPM4 is critically involved in migration of BMMCs by regulation of Ca2+-dependent actin cytoskeleton rearrangements.

AB - We demonstrate here that the transient receptor potential melastatin subfamily channel, TRPM4, controls migration of bone marrow-derived mast cells (BMMCs), triggered by dinitrophenylated human serum albumin (DNP-HSA) or stem cell factor (SCF). Wild-type BMMCs migrate after stimulation with DNP-HSA or SCF whereas both stimuli do not induce migration in BMMCs derived from TRPM4 knockout mice (trpm4-/-). Mast cell migration is a Ca2+-dependent process, and TRPM4 likely controls this process by setting the intracellular Ca2+ level upon cell stimulation. Cell migration depends on filamentous actin (F-actin) rearrangement, since pretreatment with cytochalasin B, an inhibitor of F-actin formation, prevented both DNP-HSA- and SCF-induced migration in wild-type BMMC. Immunocytochemical experiments using fluorescence-conjugated phalloidin demonstrate a reduced level of F-actin formation in DNP-HSA-stimulated BMMCs from trpm4-/- mice. Thus, our results suggest that TRPM4 is critically involved in migration of BMMCs by regulation of Ca2+-dependent actin cytoskeleton rearrangements.

KW - Actin cytoskeleton

KW - Antigen

KW - Mast cells

KW - Migration

KW - TRP channel

KW - TRPM4

KW - Transgenic mice

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U2 - 10.1016/j.ceca.2008.10.005

DO - 10.1016/j.ceca.2008.10.005

M3 - 学術論文

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AN - SCOPUS:61449093870

SN - 0143-4160

VL - 45

SP - 226

EP - 232

JO - Cell Calcium

JF - Cell Calcium

IS - 3

ER -

TRPM4 regulates migration of mast cells in mice

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