TRPM7 in cerebral ischemia and potential target for drug development in stroke

Bae, Christine You-jin; Sun, Hong‐Shuo

doi:10.1038/aps.2011.60

Cited by 41 publications

(29 citation statements)

References 87 publications

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“…In T cells, MAGT1 is activated by TCR stimulation, although the mechanisms of activation remain unknown (75). TRPM7 is a Mg 2+ -permeable, nonselective channel that conducts Ca 2+ and other divalent cations including Ca 2+ , Zn 2+ , and Ni 2+ (78, 79). TRPM7 is ubiquitously expressed and is thought to regulate cellular and organismal Mg 2+ homeostasis due to its high Mg 2+ permeability.…”

Section: Ion Channels and Transporters Regulating Immune Functionmentioning

confidence: 99%

Ion Channels in Innate and Adaptive Immunity

Feske¹,

Wulff

Skolnik

2015

Annu. Rev. Immunol.

597

616

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Ion channels and transporters mediate the transport of charged ions across hydrophobic lipid membranes. In immune cells, divalent cations such as calcium, magnesium, and zinc have important roles as second messengers to regulate intracellular signaling pathways. By contrast, monovalent cations such as sodium and potassium mainly regulate the membrane potential, which indirectly controls the influx of calcium and immune cell signaling. Studies investigating human patients with mutations in ion channels and transporters, analysis of gene-targeted mice, or pharmacological experiments with ion channel inhibitors have revealed important roles of ionic signals in lymphocyte development and in innate and adaptive immune responses. We here review the mechanisms underlying the function of ion channels and transporters in lymphocytes and innate immune cells and discuss their roles in lymphocyte development, adaptive and innate immune responses, and autoimmunity, as well as recent efforts to develop pharmacological inhibitors of ion channels for immunomodulatory therapy.

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Section: Ion Channels and Transporters Regulating Immune Functionmentioning

confidence: 99%

Ion Channels in Innate and Adaptive Immunity

Feske¹,

Wulff

Skolnik

2015

Annu. Rev. Immunol.

597

616

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“…release from intracellular stores (29). Physiological redox transitions required for stem cell differentiation and gene expression during embryonic development (30,31) may also be sensed by TRPM7 and transduced via Zn -dependent signals (32).…”

Section: +mentioning

confidence: 99%

TRPM7 senses oxidative stress to release Zn ²⁺ from unique intracellular vesicles

Abiria

Krapivinsky

Sah

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

104

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TRPM7 (transient receptor potential cation channel subfamily M member 7) regulates gene expression and stress-induced cytotoxicity and is required in early embryogenesis through organ development. Here, we show that the majority of TRPM7 is localized in abundant intracellular vesicles. These vesicles (M7Vs) are distinct from endosomes, lysosomes, and other familiar vesicles or organelles. , an ion channel and cytoplasmic kinase, is ubiquitously expressed and essential in early embryonic development (1-4) but also may mediate oxidative stress-induced anoxic neuronal death in adults (5, 6). As an ion channel, TRPM7 conducts Zn 2+ >Mg 2+ ∼ Ca 2+ and monovalent cations (7-10) and contributes to labile cytosolic and nuclear Zn 2+ concentrations (8). TRPM7's C-terminal kinase can phosphorylate multiple substrates (11-13) and is cleaved to release a proapoptotic, chromatin-modifying enzyme (8,14). Zn 2+ regulates TRPM7's kinase activity (11) and binding to transcription factors (8). It is a potent signal for many cellular processes previously related to TRPM7 function, including gene expression, mitosis, and cell survival, but is also proapoptotic at extreme concentrations (15)(16)(17)(18) Oxidative stress increases inward divalent ion permeation through TRPM7 (5, 9), whereas acute and chronic oxidative stress in culture (24-26) or during ischemia-reperfusion in vivo (27, 28) induces TRPM7 expression. The resulting increase in cytosolic Zn 2+ could result in toxic cytosolic concentrations (9). Conversely, reduction of TRPM7 expression protects animals from postischemia reperfusion (5), a condition typically accompanied by increased reactive oxygen species (ROS) and Zn 2+ release from intracellular stores (29). Physiological redox transitions required for stem cell differentiation and gene expression during embryonic development (30, 31) may also be sensed by TRPM7 and transduced via Zn -dependent signals (32). Because TRPM7 patch-clamp recording is limited to the plasma membrane, the assumption has been that TRPM7's main function is on the plasma membrane. However, we have previously shown that TRPM7 is also on intracellular membranes (33-35). Indeed, ROS activation of divalent ion influx through TRPM7 (5, 9) is reminiscent of ROS activation of TRPM2, which releases Ca 2+ and Zn 2+ from lysosomes (36,37 ] and ROS during development and injury.

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“…TRPM7 belongs to the melastatin-related subfamily of TRP channels, which contains eight members, designated TRPM1-8. It is ubiquitously expressed in almost all tissues, including neuronal cells (Bae and Sun, 2011), and is permeable to a wide range of divalent metal ions such as Zn 2þ , Mg 2þ , Mn 2þ and Ca 2þ (Monteilh-Zoller et al, 2003). Activation of TRPM7 was shown to be implicated in playing direct roles in Ca 2þ -mediated neuronal death, but the underlying mechanism was not fully understood (Aarts et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Carvacrol attenuates traumatic neuronal injury through store-operated Ca2+ entry-independent regulation of intracellular Ca2+ homeostasis

Zhang

Zhou

et al. 2015

Neurochemistry International

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TRPM7 in cerebral ischemia and potential target for drug development in stroke

Cited by 41 publications

References 87 publications

Ion Channels in Innate and Adaptive Immunity

Ion Channels in Innate and Adaptive Immunity

TRPM7 senses oxidative stress to release Zn ²⁺ from unique intracellular vesicles

Carvacrol attenuates traumatic neuronal injury through store-operated Ca2+ entry-independent regulation of intracellular Ca2+ homeostasis

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TRPM7 in cerebral ischemia and potential target for drug development in stroke

Cited by 41 publications

References 87 publications

Ion Channels in Innate and Adaptive Immunity

Ion Channels in Innate and Adaptive Immunity

TRPM7 senses oxidative stress to release Zn 2+ from unique intracellular vesicles

Carvacrol attenuates traumatic neuronal injury through store-operated Ca2+ entry-independent regulation of intracellular Ca2+ homeostasis

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Product

Resources

About

TRPM7 senses oxidative stress to release Zn ²⁺ from unique intracellular vesicles