TRPM channels, calcium and redox sensors during innate immune responses

Massullo, Pam; Sumoza-Toledo, Adriana; Bhagat, Harivadan; Partida-Sánchez, Santiago

doi:10.1016/j.semcdb.2006.11.006

Cited by 82 publications

(63 citation statements)

References 129 publications

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“…Notably, the fMLP-induced Ca 2+ response and in vitro migration were suppressed in Trpm2-deficient neutrophils. This supports the idea that fMLP activates CD38 to induce cADPR and ADPR production and the Ca 2+ influx via TRPM2 required for neutrophil chemotaxis 15 , in contrast to the CXCL2-induced neutrophil chemotaxis that does not receive a significant contribution from TRPM2 channels and that is probably mediated by classical inositol triphosphate-induced Ca 2+ release and possibly store-operated Ca 2+ entry. It will be useful to study which type of signaling mechanism other chemokines employ in inducing chemotaxis.…”

Section: Discussionsupporting

confidence: 82%

“…TRPM2, a member of the TRPM subfamily, is a Ca 2+ -permeable channel activated by intracellular messengers such as ADP-ribose (ADPR), nicotinamide adenine dinucleotide (NAD + ) and cyclic ADPR (cADPR) [13][14][15] . TRPM2 is abundantly expressed in inflammatory cells including monocytes, neutrophils and T lymphocytes [13][14][15] . We have reported that TRPM2 acts also as a sensor for ROS and oxidative stress 14 .…”

mentioning

confidence: 99%

“…The ROS sensitivity of TRPM2 can be mediated by NAD + (ref. 14 ) or ADPR 15 released from mitochondria 16 or through direct protein oxidation 15 . H 2 O 2 and cADPR have been proposed to potentiate the effects of ADPR at lower concentrations and to gate the TRPM2 channel directly at higher concentrations 15 .…”

mentioning

confidence: 99%

“…14 ) or ADPR 15 released from mitochondria 16 or through direct protein oxidation 15 . H 2 O 2 and cADPR have been proposed to potentiate the effects of ADPR at lower concentrations and to gate the TRPM2 channel directly at higher concentrations 15 . It has been suggested that H 2 O 2 -activated Ca 2+ influx through TRPM2 mediates pathophysiological cell death 14,17 .…”

mentioning

confidence: 99%

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TRPM2-mediated Ca2+ influx induces chemokine production in monocytes that aggravates inflammatory neutrophil infiltration

Yamamoto

Shimizu

Kiyonaka

et al. 2008

Nat Med

528

532

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Reactive oxygen species (ROS) induce chemokines responsible for the recruitment of inflammatory cells to sites of injury or infection. Here we show that the plasma membrane Ca 2+ -permeable channel TRPM2 controls ROS-induced chemokine production in monocytes. In human U937 monocytes, hydrogen peroxide (H 2 O 2 ) evokes Ca 2+ influx through TRPM2 to activate Ca 2+ -dependent tyrosine kinase Pyk2 and amplify Erk signaling via Ras GTPase. This elicits nuclear translocation of nuclear factor-κB essential for the production of the chemokine interleukin-8 (CXCL8). In monocytes from Trpm2-deficient mice, H 2 O 2 -induced Ca 2+ influx and production of the macrophage inflammatory protein-2 (CXCL2), the mouse CXCL8 functional homolog, were impaired. In the dextran sulfate sodium-induced colitis inflammation model, CXCL2 expression, neutrophil infiltration and ulceration were attenuated by Trpm2 disruption. Thus, TRPM2 Ca 2+ influx controls the ROS-induced signaling cascade responsible for chemokine production, which aggravates inflammation. We propose functional inhibition of TRPM2 channels as a new therapeutic strategy for treating inflammatory diseases.

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Section: Discussionsupporting

confidence: 82%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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TRPM2-mediated Ca2+ influx induces chemokine production in monocytes that aggravates inflammatory neutrophil infiltration

Yamamoto

Shimizu

Kiyonaka

et al. 2008

Nat Med

528

532

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“…CD38 hydrolyzes cADPR to ADPR through its cADPR hydrolase activity. These end products are active biologically as second messengers: cADPR gates Ca 2+ release from intracellular stores, and ADPR can activate the transient receptor potential (TRP) channel-2 leading to Ca 2+ influx (8,9). As a receptor, CD38 is involved in the transduction of activation and proliferation signals, thus cooperat- …”

Section: Introductionmentioning

confidence: 99%

CD38 and CD157 Ectoenzymes Mark Cell Subsets in the Human Corneal Limbus

Horenstein

Sizzano

Lusso

et al. 2009

Mol Med

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TRPChannels

Gees

Owsianik

Nilius

et al. 2012

Comprehensive Physiology

142

110

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TRP channels constitute a large superfamily of cation channel forming proteins, all related to the gene product of the transient receptor potential (trp) locus in Drosophila. In mammals, 28 different TRP channel genes have been identified, which exhibit a large variety of functional properties and play diverse cellular and physiological roles. In this article, we provide a brief and systematic summary of expression, function, and (patho)physiological role of the mammalian TRP channels.

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TRPM channels, calcium and redox sensors during innate immune responses

Cited by 82 publications

References 129 publications

TRPM2-mediated Ca2+ influx induces chemokine production in monocytes that aggravates inflammatory neutrophil infiltration

TRPM2-mediated Ca2+ influx induces chemokine production in monocytes that aggravates inflammatory neutrophil infiltration

CD38 and CD157 Ectoenzymes Mark Cell Subsets in the Human Corneal Limbus

TRPChannels

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