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To determine the differentially expressed genes in cancer associated fibroblasts upon ablation of the glutamatergic synapse protein NetrinG1. [Microarray]

ABSTRACT: Cancer associated fibroblast mRNA profiles were generated from Control and NetrinG1 KO fibroblast lines, with controls done in duplicate and KOs in triplicate. Comparing the mRNA profiles of CON and NetrinG1 KO CAFs, we observed a reversion of many pro-tumor genes and associated pathways upon ablation of NetrinG1 in CAFs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE156962 | GEO | 2020/08/28

REPOSITORIES: GEO

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To determine the differentially expressed genes in cancer associated fibroblasts upon ablation of the glutamatergic synapse protein NetrinG1. [RNA-Seq]

Project description:Purpose: To determine the differentially expressed genes in cancer associated fibroblasts upon ablation of the glutamatergic synapse protein NetrinG1. Methods: Cancer associated fibroblast mRNA profiles were generated from Control and NetrinG1 KO fibroblast lines, with controls done in duplicate and KOs in triplicate. Results: Comparing the mRNA profiles of CON and NetrinG1 KO CAFs, we observed a reversion of many pro-tumor genes and associated pathways upon ablation of NetrinG1 in CAFs. Conclusions: Loss of NetrinG1 in CAFs results in normalization of CAF gene signatures.

2020-08-28 | GSE156963 | GEO

SIRT6 regulates glucose metabolism and glutamatergic synapse in the mouse retina

Project description:Microarray analysis on total retinal RNA from 15 day old Sirt6 wild-type (WT) and knock-out (KO) mice. The retina is one of the major energy consuming tissues within the body. In this context, synaptic transmission between light-excited rod photoreceptors and downstream ON-bipolar neurons is a highly demanding energy consuming process. Sirtuin 6 (SIRT6), a NAD-dependent deacylase, plays a key role in regulating glucose metabolism. In this study, we demonstrate that SIRT6 is highly expressed in the retina, controlling levels of histone H3K9 and H3K56 acetylation. Notably, despite apparent normal histology, SIRT6 deficiency caused major retinal transmission defects concomitant to changes in expression of glycolytic genes and glutamate receptors, as well as elevated levels of apoptosis in inner retina cells. Our results identify SIRT6 as a critical modulator of retinal function, likely through its effects on chromatin. Microarray analysis of total retinal RNA from 15 day old Sirt6 wild-type (WT) and knock-out (KO) mice with 3 replicates in each condition using the Affymetrix Mouse Gene 2.1 ST array (transcript (gene) version).

2014-07-30 | E-GEOD-56563 | biostudies-arrayexpress

To determine the differentially expressed genes in cancer associated fibroblasts upon ablation of the glutamatergic synapse protein NetrinG1.

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-08-28 | GSE156964 | GEO

SIRT6 regulates glucose metabolism and glutamatergic synapse in the mouse retina

2014-07-30 | GSE56563 | GEO

Postsynaptic ephrinB3 promotes shaft glutamatergic synapse formation.

Project description:Excitatory synapses in the CNS are formed on both dendritic spines and shafts. Recent studies show that the density of shaft synapses may be independently regulated by behavioral learning and the induction of synaptic plasticity, suggesting that distinct mechanisms are involved in regulating these two types of synapses. Although the molecular mechanisms underlying spinogenesis and spine synapse formation are being delineated, those regulating shaft synapses are still unknown. Here, we show that postsynaptic ephrinB3 expression promotes the formation of glutamatergic synapses specifically on the shafts, not on spines. Reducing or increasing postsynaptic ephrinB3 expression selectively decreases or increases shaft synapse density, respectively. In the ephrinB3 knock-out mouse, although spine synapses are normal, shaft synapse formation is reduced in the hippocampus. Overexpression of glutamate receptor-interacting protein 1 (GRIP1) rescues ephrinB3 knockdown phenotype by restoring shaft synapse density. GRIP1 knockdown prevents the increase in shaft synapse density induced by ephrinB3 overexpression. Together, our results reveal a novel mechanism for independent modulation of shaft synapses through ephrinB3 reverse signaling.

| S-EPMC6672605 | biostudies-literature

Tissue-specific modifier alleles determine Mertk loss-of-function traits

Project description:Knockout (KO) mouse models play critical roles in elucidating biological processes behind disease-associated or disease-resistant traits. As a consequence of gene KO, mice display certain phenotypes. Based on insight into the molecular role of said gene in a biological process, it is inferred that the particular biological process causally underlies the trait. This approach has been crucial towards understanding the basis of pathological and/or advantageous traits associated with Mertk KO. MERTK is a receptor tyrosine kinase with a critical role in phagocytosis of apoptotic cells or cellular debris. Therefore, early-onset, severe retinal degeneration was described to be a direct consequence of failed phagocytosis of photoreceptor outer segments by retinal pigment epithelia. Similarly, enhanced anti-tumor immunity was inferred to result from the failure of macrophages to dispose cancer cell corpses, resulting in a pro-inflammatory tumor microenvironment. Here we report that the loss of Mertk alone is not sufficient for retinal degeneration. This trait only manifests when the function of the paralog Tyro3 is concomitantly lost. Additionally, the dramatic resistance against two syngeneic mouse tumor models observed in Mertk KO cannot, at least entirely, be ascribed to the loss of Mertk. The widely used Mertk KO carries multiple coincidental changes in its genome that affect the expression of a number of genes, including Tyro3. Nonetheless, neither Tyro3, nor macrophage phagocytosis by alternate genetic redundancy, accounts for the absence of anti-tumor immunity in two independent Mertk KOs. Collectively, our results indicate that context-dependent epistasis of independent modifier alleles determine Mertk KO traits.

2022-08-26 | GSE205070 | GEO

Genetic ablation of either G6P-isomerase or dual LDHA/B in colon cancer cells LS174T , +/- MPP+ (1-methyl-4-phenylpyridinium)

Project description:In this study we explore the genomic re-wiring of a human colon cancer cell line (LS174T) in which fermentative glycolysis has been fully suppressed by CRISPR/Cas9 to disrupt glucose-6-phosphate isomerase (GPI-KO) or dual disruption of lactate dehydrogenases A and B (LDHAB-DKO). The effects of both KOs, had no effect on loss of viable cell function, corresponding to high concentrations of ATP production vs WT. All three clones were evaluated for transcriptomic changes using GeneChip™ Human Gene 2.1 ST Arrays by Affymetrix Inc assessing for mRNAs and long intergenic non-coding RNA transcripts.

2020-04-25 | GSE149289 | GEO

MeCP2 controls excitatory synaptic strength by regulating glutamatergic synapse number.

Project description:MeCP2 is a transcriptional repressor critical for normal neurological function. Prior studies demonstrated that either loss or doubling of MeCP2 results in postnatal neurodevelopmental disorders. To understand the impact of MeCP2 expression on neuronal function, we studied the synaptic properties of individual neurons from mice that either lack or express twice the normal levels of MeCP2. Hippocampal glutamatergic neurons that lack MeCP2 display a 46% reduction in synaptic response, whereas neurons with doubling of MeCP2 exhibit a 2-fold enhancement in synaptic response. Further analysis shows that these changes were primarily due to the number of synapses formed. These results reveal that MeCP2 is a key rate-limiting factor in regulating glutamatergic synapse formation in early postnatal development and that changes in excitatory synaptic strength may underlie global network alterations in neurological disorders due to altered MeCP2 levels.

| S-EPMC2198899 | biostudies-literature

To determine the differentially expressed genes in cancer associated fibroblasts upon ablation of the glutamatergic synapse protein NetrinG1.

Project description:To determine the differentially expressed genes in cancer associated fibroblasts upon ablation of the glutamatergic synapse protein NetrinG1.

| PRJNA659658 | ENA

An Immunological Synapse Formation Between T Regulatory Cells and Cancer-Associated Fibroblasts Promotes Tumour Development: Secretomics

Project description:Cancer-associated fibroblasts (CAFs) have emerged as a dominant non-hematopoietic cell population in the tumour microenvironment (TME), serving diverse functions in tumour progression, invasion, matrix remodelling and resistance to therapy. Extensive molecular characterization revealed an increased heterogeneity in the CAF compartment and proposed an interaction between CAFs and tumour-infiltrating immune cells, which may shape tumour immune evasion. However, the precise mechanisms via which CAFs imprint on anti-tumour immunity remain poorly understood. Herein, we describe a synapse formation between α-SMA+ CAFs and regulatory T cells (Tregs) in the TME. Specifically, Foxp3+ Tregs were localized close to α-SMA+ CAFs in diverse types of tumour models as well as in biopsies from melanoma and colorectal cancer patients. Notably, α-SMA+ CAFs demonstrated the ability to phagocytose and process tumour antigens and exhibited a tolerogenic phenotype which instructed a Treg cell movement arrest with Treg cell activation and proliferation, in an antigen-specific manner. Of interest, α-SMA+ CAFs were characterized by the presence of double-membrane structures, resembling autophagosomes, in their cytoplasm, while analysis of single-cell transcriptomic data pointed autophagy and antigen processing/presentation pathways to be enriched in α-SMA-expressing CAF clusters. In a mechanistic view, conditional knockout of the autophagy pathway in α-SMA+ CAFs promoted an inflammatory re-programming of CAFs, reduced Treg cell infiltration, attenuated tumour development, and potentiated the efficacy of immune checkpoint inhibitor immunotherapy. Overall, our findings reveal an immunosuppressive mechanism operating in the TME, which entails the formation of synapses between α-SMA+ CAFs and Tregs in an autophagy-dependent fashion and raises the potential for the development of CAF-targeted therapies in cancer. Here we submit the secretome proteomic analyses.

2024-05-08 | PXD047038 | Pride

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