GPR35 regulates anxiety susceptibility
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB84375 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Mutations in GPR35 (G protein coupled receptor 35) are linked to ulcerative colitis and primary sclerosing cholangitis. How GPR35, which interacts with the Na/K-ATPase to determine ion transport, influences the transcriptome of macrophages and the ileum is unknown. Here compare transcript expression in bone marrow-derived macrophages and isolated ileum from mice deficient in GPR35 (knockout) with wild type mice by bulk RNA sequencing.
2025-02-07 | GSE252926 | GEO
Project description:Aim: We aimed to determine differences in transcriptional profiles of GPR35-positive and negative macrophages in the steady state intestine. Method: Corresponding subpopulations were sorted by FACS from intestinal lamina propria cells of unmanipulated wild-type C56BL/6 mice. RNA from 4 replicates of each group were sequenced and analyzed. Result: GPR35 positive macrophages are transcriptionally distinct from GPR35 negative macrophages overall with 2798 downregulated and 2773 upregulated genes, and regarding cytokine expression profile with higher Il1b, Tnf and Il10 mRNA expressions. Conclusion: Our study reports the first analysis on transcriptional charasteristics of intestinal macrophages depending on their GPR35 expression providing insights into the function of GPR35 in these cells.
2020-06-25 | GSE131858 | GEO
Project description:Purpose: Our previous experiments showed that LPA activated inhibitory G-protein signaling in human GPR35-transfected cells. We wanted to test the LPA signaling in presence or absence of GPR35. Methods: We isolated RNA from bone-marrow derived macrophages (BMDMs) from WT or GPR35-deficient mice that were treated with LPA or LPS, and left untreated for control. Results: We have found that GPR35-deficiency alters the transcriptional profiles in response to LPA in BMDMs. On the other hand, LPS-treated WT and GPR35-deficient BMDMs showed similar transcriptional changes. Conclusion: GPR35-deficientcy alters the LPA but not LPS signaling.
2020-06-23 | GSE153012 | GEO
Project description:We performed a single-cell transcriptome analysis of proximal colon epithelial cells from 4 Gpr35 KO and 4 WT female littermates mice at a steady state.
2022-03-22 | GSE169183 | GEO
Project description:Trait anxiety is one of the major contributors to susceptibility to stress-induced and anxiety disorders in humans. Although vulnerability to stress-induced pathologies is clearly highly individual, animal models still largely fail to account for it. Using the threat imminence continuum theory, we designed and validated an experimental pipeline in mice centred around auditory aversive conditioning. Harnessing the naturally occurring variability of defensive freezing responses combined with a model-based clustering strategy enabled us to operationalize trait anxiety. We identified sustained freezing during prolonged retrieval sessions as a behavioural marker of an anxiety endophenotype in both males and females. RNA-sequencing of key defence circuit brain regions revealed massive differences in transcriptomes of phasic and sustained responders, correlating with transcriptomic signatures of psychiatric disorders such as PTSD and schizophrenia. We provide compelling evidence that trait anxiety in inbred mice can be leveraged to develop translationally relevant preclinical models to investigate mechanisms of stress susceptibility.
2024-04-09 | GSE223269 | GEO
Project description:We used human embryonic kidney HEK293T cells transfected with human GPR35 cDNAs as baits that were engineered to express Strep or hemagglutinin (HA) tags at the C terminus to perform an unbiased proteomics survey for GPR35 interaction partners.
2019-11-12 | PXD011269 | Pride
Project description:OGFOD1 Regulates Translation to Alter Hypertrophy Susceptibility
| PRJNA900269 | ENA
Project description:Our study represents the first detailed analysis of transcriptomes between poststroke anxiety and General Anxiety by RNA-seq technology. We founded that: compared with pure restraint stress, stroke plus restraint stress leaded to other pathways: 1) Oxidative stress and redox pathways are out-of-balance; 2). Production of nitric oxide is disordered; 3). Mitochondrial ATP synthesis is coupled with electron transport pathway dysfunction. These upregulated genes analyzed integrally were greatly enriched in the regulation of cytokine production, inflammatory response and leukocyte infiltration. And our results detailly predicted downstream transcriptional differences with HDAC3 inhibitor treatment or not in poststroke anxiety. We concluded that HDAC3-regulated PGE2 production by microglia constitutes phobic anxiety susceptibility after stroke.
2022-01-28 | GSE194326 | GEO
Project description:Mass spectrometry, mutagenesis and labelling with [32P] orthophosphate identified that each of the five hydroxy-amino acids in the intracellular C-terminal tail of human GPR35a became phosphorylated in response to agonist occupancy of the receptor and that, apart from Ser294, each of these contributed to the effectiveness of interaction of the receptor with arrestin-3. Key to such interactions was Ser303. Despite there being a greater number of hydroxy-amino acids in the C-terminal tail of both mouse and rat GPR35 the serine corresponding to residue 303 in human GPR35a also played a dominant role in arrestin-3 interactions for both rodent orthologues. Fully phospho-site deficient mutants of human GPR35a and mouse GPR35 failed to interact effectively with arrestin-3 and the human phospho-deficient variant was not internalized from the surface of cells in response to agonist treatment. Even in cells stably expressing species orthologues of GPR35 a substantial proportion of the expressed protein(s) was, however, immature. Phospho-site specific antisera targeting the region encompassing Ser303 in human (Ser301 in mouse) GPR35 identified only the mature forms of GPR35 and provided effective biomarkers of the activation status of the receptors both in immunoblotting and immunocytochemical studies. Such antisera may be useful tools to evaluate target engagement in drug discovery and target validation programmes.
2022-04-04 | PXD030548 | Pride
Project description:Emerging evidence has shown that noncoding RNAs, particularly microRNAs (miRNAs), contribute to the pathogenesis of mood and anxiety disorders, although the molecular mechanisms are poorly understood. Here we show altered levels of miR-17-92 in adult hippocampal neural progenitors have a significant impact in neurogenesis and anxiety- and depression-related behaviors in mice. miR-17-92 deletion in adult neural progenitors causes a decrease, while its overexpression an increase of neurogenesis in the dentate gyrus, through regulating genes in the glucocorticoid pathway, especially serum- and glucocorticoid-inducible protein kinase-1 (Sgk1). miR-17-92 knockout mice show anxiety- and depression-like behaviors, whereas miR-17-92 overexpressing mice exhibit anxiolytic and antidepression-like behaviors. Furthermore, we show that miR-17-92 expression in the adult mouse hippocampus responds to chronic stress, and miR-17-92 rescues proliferation defects, induced by corticosterone, in hippocampal neural progenitors. Our study uncovers a crucial role for miR-17-92 in adult neural progenitors to regulate neurogenesis and anxiety- and depression-like behaviors.
2016-12-09 | GSE83636 | GEO