Trpm1

Irie, Satoshi; Furukawa, Takahisa

doi:10.1007/978-3-642-54215-2_15

Cited by 19 publications

(22 citation statements)

References 81 publications

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“…Similarly, differences were evident in the comparison of top DE mRNAs differentiating peri‐implantitis and periodontitis from healthy gingival tissues. Peri‐implantitis lesions showed a distinct down‐regulation of melan‐A, a melanocytic marker, and TRPM‐1/melastatin, also expressed on melanocytes, consistent with the presence of melanocytes in the periodontal ligament, which is lacking in peri‐implant tissue, and may suggest these cells play a distinct immunologic role in periodontal inflammation. Comparing periodontitis and health, the most up‐regulated GO term was “T‐helper 17 cell lineage commitment,” in agreement with previous studies, these results implied Th17 immune response as having a key role in periodontitis.…”

Section: Discussionsupporting

confidence: 56%

Long non‐coding RNA and mRNA expression profiles in peri‐implantitis vs periodontitis

Liu

et al. 2019

J of Periodontal Research

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Background and Objective:Peri-implantitis is a biofilm-mediated infectious disease that results in progressive loss of implant-supporting bone. As compared to its analogue periodontitis, peri-implantitis is generally known to be more aggressive, with comparatively rapid progression and less predictable treatment outcomes, especially when advanced. An understanding of molecular mechanisms underpinning the similarities and differences between peri-implantitis and periodontitis is essential to develop novel management strategies. This study aimed to compare long non-coding RNAs (lncRNAs) and messenger RNA (mRNA) expression profiles between peri-implantitis and periodontitis.Methods: Inflamed soft tissue from peri-implantitis and periodontitis lesions, and healthy gingival tissue controls were analyzed by microarray. Cluster graphs, gene ontology (GO) analysis, and pathway analysis were performed. Quantitative real-time PCR was employed to verify microarray results. The expression levels of RANKL and OPG in the three tissue types were also evaluated, using qRT-PCR. Coding non-coding (CNC) network analyses were performed.Results: Microarray analyses revealed 1079 lncRNAs and 1003 mRNAs as differentially expressed in peri-implantitis when compared to periodontitis. The cyclooxygenase-2 pathway was the most up-regulated biological process in peri-implantitis as compared to periodontitis, whereas hemidesmosome assembly was the most down-regulated pathway. Osteoclast differentiation was relatively up-regulated, and RANKL/OPG ratio was higher in peri-implantitis than in periodontitis. Conclusions:The study demonstrated that peri-implantitis and periodontitis exhibit significantly different lncRNA and mRNA expression profiles, suggesting that osteoclast differentiation-related pathways are comparatively more active in periimplantitis. These data highlight potential molecular targets for periodontitis and peri-implantitis therapy development. K E Y W O R D SlncRNA, microarray, peri-implantitis, periodontitis, transcriptome | 343 LIU et aL.

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Section: Discussionsupporting

confidence: 56%

Long non‐coding RNA and mRNA expression profiles in peri‐implantitis vs periodontitis

Liu

et al. 2019

J of Periodontal Research

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“…The TRPM1 channel is the founding member of this subfamily, and its sequence is similar to that of other members of the TRP family of cation channels (Irie and Furukawa, ). TRPM1 channels are found primarily in melanin‐producing cells, including melanocytes (Fang and Setaluri, ; Zhiqi et al , ).…”

Section: Function Of Trp Channels In Immune and Inflammatory Cellsmentioning

confidence: 95%

What is the evidence for the role of TRP channels in inflammatory and immune cells?

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Geppetti

et al. 2016

British J Pharmacology

131

121

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A complex network of many interacting mechanisms orchestrates immune and inflammatory responses. Among these, the cation channels of the transient receptor potential (TRP) family expressed by resident tissue cells, inflammatory and immune cells and distinct subsets of primary sensory neurons, have emerged as a novel and interrelated system to detect and respond to harmful agents. TRP channels, by means of their direct effect on the intracellular levels of cations and/or through the indirect modulation of a large series of intracellular pathways, orchestrate a range of cellular processes, such as cytokine production, cell differentiation and cytotoxicity. The contribution of TRP channels to the transition of inflammation and immune responses from a defensive early response to a chronic and pathological condition is also emerging as a possible underlying mechanism in various diseases. This review discusses the roles of TRP channels in inflammatory and immune cell function and provides an overview of the effects of inflammatory and immune TRP channels on the pathogenesis of human diseases.Abbreviations ADPR, ADP ribose; APC, antigen presenting cell; BMMCs, bone marrow-derived mast cells; cADPR, cyclic ADPR; COPD, chronic obstructive pulmonary disease; CRAC, Ca 2+ -release activated channel; DCs, dendritic cells; EAE, experimental autoimmune encephalomyelitis; fMLP, fMet-Leu-Phe peptide; MCs, mast cells; NAADP, nicotinic acid adenine dinucleotide phosphate; NOX, NADPH oxidase; ORAI1, Ca 2+ -release-activated Ca 2+ channel protein 1; PMNs, polymorphonuclear neutrophil granulocytes; SOCE, store-operated calcium entry; STIM1, stromal interaction molecule 1; TCR, T-cell receptor Tables of Links TARGETS Voltage-gated Ion Channels TRPM1 TRPV1 TRPA1 TRPM2 TRPV2 TRPC1 TRPM4 TRPV4 TRPC3 TRPM5 TRPV5 TRPC5 TRPM7 TRPV6 TRPC6 TRPM8 Dendritic cellsDendritic cells (DCs), the most efficient APCs, are the first orchestrators of the immune response, given that they patrol the environment throughout the body and determine whether and how an immune response should be initiated (Lipscomb and Masten, 2002). DCs are specifically able to process, interpret and, finally, communicate the nature of the pathogenic stimulus to initiate all antigen-driven immune responses (Banchereau and Steinman, 1998). DCs capture and process pathogenic antigens, express costimulatory molecules that are able to enhance the T-cell response, secrete stimulatory cytokines and are involved in the maintenance of the immune tolerance (the ability of immune system to not produce immune responses against self-antigens or non-pathogenic environmental antigens) (Mellman, 2013). Pathogenic stimuli switch immature DCs, adept at antigen accumulation, to mature DCs, specialized for T-cell stimulation, which express a high level of antigen-presenting and co-stimulatory molecules and cytokines, and migrate to lymph nodes. PMNsPMNs are key players in inflammatory processes. Monocytes and macrophagesMacrophages and their precursors, monocytes, have ...

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“…3) harboring a heptad repeat pattern of hydrophobic and polar or charged amino acid residues that is believed to be sufficient for tetramer self-assembly and necessary for channel function [29,58,105,106]. However, TRPM3 (and TRPM1) lacks the Cterminal enzyme domains found in the TRPM2 (pyrophosphatase), TRPM6 (kinase), and TRPM7 (kinase) channels or so-called chanzymes [58,107].…”

Section: Trpm3 Channel Structure-function Domainsmentioning

confidence: 99%

TRPM3_miR-204: a complex locus for eye development and disease

Shiels

2020

Hum Genomics

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First discovered in a light-sensitive retinal mutant of Drosophila, the transient receptor potential (TRP) superfamily of non-selective cation channels serve as polymodal cellular sensors that participate in diverse physiological processes across the animal kingdom including the perception of light, temperature, pressure, and pain. TRPM3 belongs to the melastatin sub-family of TRP channels and has been shown to function as a spontaneous calcium channel, with permeability to other cations influenced by alternative splicing and/or non-canonical channel activity. Activators of TRPM3 channels include the neurosteroid pregnenolone sulfate, calmodulin, phosphoinositides, and heat, whereas inhibitors include certain drugs, plant-derived metabolites, and G-protein subunits. Activation of TRPM3 channels at the cell membrane elicits a signal transduction cascade of mitogen-activated kinases and stimulus response transcription factors. The mammalian TRPM3 gene hosts a non-coding microRNA gene specifying miR-204 that serves as both a tumor suppressor and a negative regulator of post-transcriptional gene expression during eye development in vertebrates. Ocular co-expression of TRPM3 and miR-204 is upregulated by the paired box 6 transcription factor (PAX6) and mutations in all three corresponding genes underlie inherited forms of eye disease in humans including early-onset cataract, retinal dystrophy, and coloboma. This review outlines the genomic and functional complexity of the TRPM3_miR-204 locus in mammalian eye development and disease.

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Trpm1

Cited by 19 publications

References 81 publications

Long non‐coding RNA and mRNA expression profiles in peri‐implantitis vs periodontitis

Long non‐coding RNA and mRNA expression profiles in peri‐implantitis vs periodontitis

What is the evidence for the role of TRP channels in inflammatory and immune cells?

TRPM3_miR-204: a complex locus for eye development and disease

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