Transient Receptor Potential (TRP) Channels in Health and Disease

Dietrich, Alexander

doi:10.3390/cells8050413

Cited by 27 publications

(22 citation statements)

References 31 publications

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“…In addition, TRPC1 appears to contribute to the regulation of the epithelial-mesenchymal transition (EMT) in cancer; its inhibition suppresses TGF-β1-induced EMT 96,97 . TRPC3 is expressed in various immune cells and has been proposed to contribute to vascular inflammation [98][99][100] . Also, the brain-derived neurotrophic factor (BNDF) has the effect of upregulating TRPC3 in the cell membrane.…”

Section: Discussionmentioning

confidence: 99%

RNA-seq analysis reveals TRPC genes to impact an unexpected number of metabolic and regulatory pathways

Formoso

Susperreguy

Freichel

et al. 2020

Sci Rep

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The seven-member transient receptor potential canonical genes (TRPC1-7) encode cation channels linked to several human diseases. there is little understanding of the participation of each tRpc in each pathology, considering functional redundancy. Also, most of the inhibitors available are not specific. Thus, we developed mice that lack all of the TRPCs and performed a transcriptome analysis in eight tissues. the aim of this research was to address the impact of the absence of all tRpc channels on gene expression. We obtained a total of 4305 differentially expressed genes (DEGs) in at least one tissue where spleen showed the highest number of DEGs (1371). Just 21 genes were modified in all the tissues. Performing a pathway enrichment analysis, we found that many important signaling pathways were modified in more than one tissue, including PI3K (phosphatidylinositol 3-kinase/protein kinase-B) signaling pathway, cytokine-cytokine receptor interaction, extracellular matrix (ECM)-receptor interaction and circadian rhythms. We describe for the first time the changes at the transcriptome level due to the lack of all tRpc proteins in a mouse model and provide a starting point to understand the function of tRpc channels and their possible roles in pathologies.

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Section: Discussionmentioning

confidence: 99%

RNA-seq analysis reveals TRPC genes to impact an unexpected number of metabolic and regulatory pathways

Formoso

Susperreguy

Freichel

et al. 2020

Sci Rep

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“…Transient receptor potential (TRP) channels are known to be involved in the regulation of cell migration, adhesion, and proliferation, as well as neoangiogenesis [56]. The TRP superfamily consists of the following six subfamilies, which are based on sequence homology: ankyrin-rich (TRPA1), vanilloid (TRPV1-6), canonical (TRPC1-7), melastatin-like (TRPM1-8), polycystin (TRPP2/3/5), and mucolipin (TRPML1-3) [57].…”

Section: Transient Receptor Potential (Trp) Channels and Endometriosismentioning

confidence: 99%

“…The TRP superfamily consists of the following six subfamilies, which are based on sequence homology: ankyrin-rich (TRPA1), vanilloid (TRPV1-6), canonical (TRPC1-7), melastatin-like (TRPM1-8), polycystin (TRPP2/3/5), and mucolipin (TRPML1-3) [57]. Their localization is ubiquitary, and they can be activated by a wide number of molecules and stimuli [56,58,59]. In endometrial biopsies, TRP expression levels have been reported to be differently down-and upregulated during the different phases of the menstrual cycle [60].…”

Section: Transient Receptor Potential (Trp) Channels and Endometriosismentioning

confidence: 99%

Ion Channels in The Pathogenesis of Endometriosis: A Cutting-Edge Point of View

Riemma

Laganà

Schiattarella

et al. 2020

IJMS

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Background: Ion channels play a crucial role in many physiological processes. Several subtypes are expressed in the endometrium. Endometriosis is strictly correlated to estrogens and it is evident that expression and functionality of different ion channels are estrogen-dependent, fluctuating between the menstrual phases. However, their relationship with endometriosis is still unclear. Objective: To summarize the available literature data about the role of ion channels in the etiopathogenesis of endometriosis. Methods: A search on PubMed and Medline databases was performed from inception to November 2019. Results: Cystic fibrosis transmembrane conductance regulator (CFTR), transient receptor potentials (TRPs), aquaporins (AQPs), and chloride channel (ClC)-3 expression and activity were analyzed. CFTR expression changed during the menstrual phases and was enhanced in endometriosis samples; its overexpression promoted endometrial cell proliferation, migration, and invasion throughout nuclear factor kappa-light-chain-enhancer of activated B cells-urokinase plasminogen activator receptor (NFκB-uPAR) signaling pathway. No connection between TRPs and the pathogenesis of endometriosis was found. AQP5 activity was estrogen-increased and, through phosphatidylinositol-3-kinase and protein kinase B (PI3K/AKT), helped in vivo implantation of ectopic endometrium. In vitro, AQP9 participated in extracellular signal-regulated kinases/p38 mitogen-activated protein kinase (ERK/p38 MAPK) pathway and helped migration and invasion stimulating matrix metalloproteinase (MMP)2 and MMP9. ClC-3 was also overexpressed in ectopic endometrium and upregulated MMP9. Conclusion: Available evidence suggests a pivotal role of CFTR, AQPs, and ClC-3 in endometriosis etiopathogenesis. However, data obtained are not sufficient to establish a direct role of ion channels in the etiology of the disease. Further studies are needed to clarify this relationship.

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“…TRP channels have a broad distribution profile and are non-selective cation channels, with some of them being permeable for calcium. The superfamily of TRP channels consists of 28 members in humans, which are organized in six subgroups: TRPA, with A for "ankyrin"; TRPC, with C for "canonical", TRPM, with M for "melastatin", TRPML, with ML for "mucolipidin", TRPP, with P for "polycystin" and TRPV, with V for "vanilloid" [87].…”

Section: Trp Channelsmentioning

confidence: 99%

Strategies for Neuroprotection in Multiple Sclerosis and the Role of Calcium

Enders

Heider

Ludwig

et al. 2020

IJMS

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Calcium ions are vital for maintaining the physiological and biochemical processes inside cells. The central nervous system (CNS) is particularly dependent on calcium homeostasis and its dysregulation has been associated with several neurodegenerative disorders including Parkinson's disease (PD), Alzheimer's disease (AD) and Huntington's disease (HD), as well as with multiple sclerosis (MS). Hence, the modulation of calcium influx into the cells and the targeting of calcium-mediated signaling pathways may present a promising therapeutic approach for these diseases. This review provides an overview on calcium channels in neurons and glial cells. Special emphasis is put on MS, a chronic autoimmune disease of the CNS. While the initial relapsing-remitting stage of MS can be treated effectively with immune modulatory and immunosuppressive drugs, the subsequent progressive stage has remained largely untreatable. Here we summarize several approaches that have been and are currently being tested for their neuroprotective capacities in MS and we discuss which role calcium could play in this regard.

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Transient Receptor Potential (TRP) Channels in Health and Disease

Abstract: Almost 25 years ago, the first mammalian transient receptor potential (TRP) channel, now named TRPC1, was cloned and published (reviewed in [...]

Cited by 27 publications

References 31 publications

RNA-seq analysis reveals TRPC genes to impact an unexpected number of metabolic and regulatory pathways

RNA-seq analysis reveals TRPC genes to impact an unexpected number of metabolic and regulatory pathways

Ion Channels in The Pathogenesis of Endometriosis: A Cutting-Edge Point of View

Strategies for Neuroprotection in Multiple Sclerosis and the Role of Calcium

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