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

Formoso, Karina; Susperreguy, Sebastián; Freichel, Marc; Birnbaumer, Lutz

doi:10.1038/s41598-020-61177-x

Cited by 12 publications

(6 citation statements)

References 131 publications

(136 reference statements)

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“…They are therefore able to mediate cellular responses to these signals and interact with important hippocampal functions. and manganese ion transport were modified in both forebrain and midbrain [50]. TRPC channels are involved in a number of mechanosensory processes [51,52]; however, recent papers seem to point out that they are more likely activated by mechanosensitive processes than directly mechanosensitive [53,54].…”

Section: Introduction: Hippocampal Circuitry and Memorymentioning

confidence: 99%

How TRPC Channels Modulate Hippocampal Function

Gualdani

Gailly

2020

IJMS

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Transient receptor potential canonical (TRPC) proteins constitute a group of receptor-operated calcium-permeable nonselective cationic membrane channels of the TRP superfamily. They are largely expressed in the hippocampus and are able to modulate neuronal functions. Accordingly, they have been involved in different hippocampal functions such as learning processes and different types of memories, as well as hippocampal dysfunctions such as seizures. This review covers the mechanisms of activation of these channels, how these channels can modulate neuronal excitability, in particular the after-burst hyperpolarization, and in the persistent activity, how they control synaptic plasticity including pre- and postsynaptic processes and how they can interfere with cell survival and neurogenesis.

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Section: Introduction: Hippocampal Circuitry and Memorymentioning

confidence: 99%

How TRPC Channels Modulate Hippocampal Function

Gualdani

Gailly

2020

IJMS

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“…All animal procedures were carried out in accordance with the NIH guidelines for the Care and Use of Laboratory Animals and approved by the Animal Welfare Committee of the University of Texas Health Science Center at Houston. TRPC1 KO ( Trpc1 –/– ) and quadruple TRPC1, C4, C5, C6 KO (QuadKO) mice (129/SvEv and C57BL/6J mixed background) were created and maintained as described ( Dietrich et al, 2007 ; Formoso et al, 2020 ); TRPC4 KO ( Trpc4 –/– ) in C57BL/6 background were generated and maintained as previously described ( Freichel et al, 2001 ).…”

Section: Methodsmentioning

confidence: 99%

Contribution of TRPC Channels in Neuronal Excitotoxicity Associated With Neurodegenerative Disease and Ischemic Stroke

Jeon

Sun

et al. 2021

Front. Cell Dev. Biol.

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The seven canonical members of transient receptor potential (TRPC) proteins form cation channels that evoke membrane depolarization and intracellular calcium concentration ([Ca2+]i) rise, which are not only important for regulating cell function but their deregulation can also lead to cell damage. Recent studies have implicated complex roles of TRPC channels in neurodegenerative diseases including ischemic stroke. Brain ischemia reduces oxygen and glucose supply to neurons, i.e., Oxygen and Glucose Deprivation (OGD), resulting in [Ca2+]i elevation, ion dyshomeostasis, and excitotoxicity, which are also common in many forms of neurodegenerative diseases. Although ionotropic glutamate receptors, e.g., N-methyl-D-aspartate receptors, are well established to play roles in excitotoxicity, the contribution of metabotropic glutamate receptors and their downstream effectors, i.e., TRPC channels, should not be neglected. Here, we summarize the current findings about contributions of TRPC channels in neurodegenerative diseases, with a focus on OGD-induced neuronal death and rodent models of cerebral ischemia/reperfusion. TRPC channels play both detrimental and protective roles to neurodegeneration depending on the TRPC subtype and specific pathological conditions involved. When illustrated the mechanisms by which TRPC channels are involved in neuronal survival or death seem differ greatly, implicating diverse and complex regulation. We provide our own data showing that TRPC1/C4/C5, especially TRPC4, may be generally detrimental in OGD and cerebral ischemia/reperfusion. We propose that although TRPC channels significantly contribute to ischemic neuronal death, detailed mechanisms and specific roles of TRPC subtypes in brain injury at different stages of ischemia/reperfusion and in different brain regions need to be carefully and systematically investigated.

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“…Recent data showed the possible role of transient receptor potential canonical (TRPC) genes by performing RNAseq analysis in mice that lack the TRPC [46]. The authors pointed out the deregulation of TRPC belonging to several metabolic pathways such as PI3K-B signaling pathway, cytokine-cytokine receptor interaction, calcium homeostasis, extracellular matrix -receptor, and circadian rhythms in several human diseases.…”

Section: Deregulation Of Calcium Signaling Pathwaymentioning

confidence: 99%

Identification of a Candidate Gene Set Signature for the Risk of Progression in IgM MGUS to Smoldering/Symptomatic Waldenström Macroglobulinemia (WM) by a Comparative Transcriptome Analysis of B Cells and Plasma Cells

Trojani

Camillo

Bossi

et al. 2021

Cancers

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Waldenström Macroglobulinemia (WM) is a B-cell lymphoma characterized by the precursor condition IgM monoclonal gammopathies of undetermined significance (IgM MGUS). We performed a gene expression profiling study to compare the transcriptome signatures of bone marrow (BM) B-cells and plasma cells of 36 WM patients, 13 IgM MGUS cases, and 7 healthy subjects used as controls (CTRLs) by Affymetrix microarray. We determined 2038 differentially expressed genes (DEGs) in CD19+ cells and 29 DEGs genes in CD138+ cells, respectively. The DEGs identified in B-cells were associated with KEGG pathways, mainly involved in hematopoietic cell lineage antigens, cell adhesion/focal adhesion/transmembrane proteins, adherens junctions, Wnt-signaling pathway, BCR-signaling pathway, calcium signaling pathway, complement/coagulation cascade, platelet activation, cytokine-cytokine receptor interactions, and signaling pathways responsible for cell cycle, apoptosis, proliferation and survival. In conclusion, we showed the deregulation of groups of genes belonging to KEGG pathways in the comparison among WM vs. IgM MGUS vs. CTRLs in B-cells. Interestingly, a small set of genes in B-cells displayed a common transcriptome expression profile between WM and IgM MGUS compared to CTRLs, suggesting its possible role in the risk of transformation of IgM MGUS to WM.

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

Cited by 12 publications

References 131 publications

How TRPC Channels Modulate Hippocampal Function

How TRPC Channels Modulate Hippocampal Function

Contribution of TRPC Channels in Neuronal Excitotoxicity Associated With Neurodegenerative Disease and Ischemic Stroke

Identification of a Candidate Gene Set Signature for the Risk of Progression in IgM MGUS to Smoldering/Symptomatic Waldenström Macroglobulinemia (WM) by a Comparative Transcriptome Analysis of B Cells and Plasma Cells

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