当前位置： SCI文献检索 > IMMUNITY期刊下所有文献 > Chanzyme TRPM7 Mediates the Ca2+ Influx Essential for Lipopolysaccharide-Induced Toll-Like Receptor 4 Endocytosis and Macrophage Activation.

Chanzyme TRPM7 Mediates the Ca2+ Influx Essential for Lipopolysaccharide-Induced Toll-Like Receptor 4 Endocytosis and Macrophage Activation.

Abstract：

:Toll-like receptors (TLRs) sense pathogen-associated molecular patterns to activate the production of inflammatory mediators. TLR4 recognizes lipopolysaccharide (LPS) and drives the secretion of inflammatory cytokines, often contributing to sepsis. We report that transient receptor potential melastatin-like 7 (TRPM7), a non-selective but Ca2+-conducting ion channel, mediates the cytosolic Ca2+ elevations essential for LPS-induced macrophage activation. LPS triggered TRPM7-dependent Ca2+ elevations essential for TLR4 endocytosis and the subsequent activation of the transcription factor IRF3. In a parallel pathway, the Ca2+ signaling initiated by TRPM7 was also essential for the nuclear translocation of NFκB. Consequently, TRPM7-deficient macrophages exhibited major deficits in the LPS-induced transcriptional programs in that they failed to produce IL-1β and other key pro-inflammatory cytokines. In accord with these defects, mice with myeloid-specific deletion of Trpm7 are protected from LPS-induced peritonitis. Our study highlights the importance of Ca2+ signaling in macrophage activation and identifies the ion channel TRPM7 as a central component of TLR4 signaling.

journal_name

Immunity

journal_title

Immunity

authors

Schappe MS,Szteyn K,Stremska ME,Mendu SK,Downs TK,Seegren PV,Mahoney MA,Dixit S,Krupa JK,Stipes EJ,Rogers JS,Adamson SE,Leitinger N,Desai BN

doi

10.1016/j.immuni.2017.11.026

subject

Has Abstract

pub_date

2018-01-16 00:00:00

pages

59-74.e5

issue

1

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(17)30527-7

journal_volume

48

pub_type

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