Role of TRPV4 in methylation of the CpG sites on miR146a promoter
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1130531 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29672546.fastq.gz | Fastqsanger.gz | |||
| SRR29672547.fastq.gz | Fastqsanger.gz | |||
| SRR29672548.fastq.gz | Fastqsanger.gz | |||
| SRR29672549.fastq.gz | Fastqsanger.gz | |||
| SRR29672550.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 11 |
Similar Datasets
Project description:Epigenetic modifications, including the role of miRs in various diseases, are key regulators of gene expression. In this study we aimed to explore whether epigenetic alterations could play a role in the TRPV4-mediated regulation of miR-146a. Here we report that there is no significant differences in the methylation status of the examined 10 CpG sites on miR146a promoter between WT and TRPV4 KO cells under LPS treatment, indicating that the regulation of miR-146a by TRPV4 may not be mediated by methylation changes at these specific sites.
2024-10-23 | GSE271253 | GEO
Project description:Abstract Background Chronic constipation is prevalent and involves both colon sensitivity and various changes in intestinal bacteria, particularly mucosa-associated microflora. Here we examined regulatory mechanisms of TRPV4 expression by co-culturing colon epithelial cell lines with intestinal bacteria and their derivatives. We also investigated TRPV4 expression in colon epithelium from patients with constipation. Methods Colon epithelial cell lines were co-cultured with various enterobacteria (bacterial components and supernatant), folate, LPS, or short chain fatty acids (SCFAs). TRPV4 expression levels and promoter DNA methylation were assessed using pyrosequencing, and microarray network analysis. For human samples, correlation coefficients were calculated and multiple regression analyses were used to examine the association between clinical background, rectal TRPV4 expression level and mucosa-associated microbiota. Results Co-culture of CCD841 cells with P. acnes, C. perfringens, or S. aureus transiently decreased TRPV4 expression but did not induce methylation. Co-culture with clinical isolates and standard strains of K. oxytoca, E. faecalis, or E. coli increased TRPV4 expression in CCD841 cells, and TRPV4 and TNF-alpha expression were increased by E. coli culture supernatants but not bacterial components. Although folate, LPS, IL-6, TNF-alpha, or SCFAs alone did not alter TRPV4 expression, TRPV4 expression following exposure to E. coli culture supernatants was inhibited by butyric acid or TNF-alphaR1 inhibitor and increased by p38 inhibitor. Microarray network analysis showed activation of TNF-alpha, cytokines, and NOD signaling. TRPV4 expression was higher in constipated patients from the terminal ileum to the colorectum, and multiple regression analyses showed that low stool frequency, frequency of defecation aids, and duration were associated with TRPV4 expression. Meanwhile, incomplete defecation, time required to defecate, and number of defecation failures per 24 hours were associated with increased E. faecalis frequency. Conclusions Colon epithelium cells had increased TRPV4 expression upon co-culture with K. oxytoca, E. faecalis, or E. coli supernatants, as well as TNFα-stimulated TNFαR1 expression via a pathway other than p38. Butyrate treatment suppressed this increase. Epithelial TRPV4 expression was increased in constipated patients, suggesting that TRPV4 together with increased frequency of E. faecalis may be involved in the pathogenesis of various constipation symptoms.
2022-07-15 | GSE208164 | GEO
Project description:Comparing gene expression profile in 3T3-F442A adipocytes with shRNA against TRPV4 or GFP. TRPV4 is an ion channel expressed in adipocytes. Results provided information that how loss-of-function of TRPV4 affects gene expression in adipocytes. 4 samples were analyzed as two groups: shGFP (control) and shTRPV4 (experimental). Each group has two replicates.
2012-10-12 | E-GEOD-40280 | biostudies-arrayexpress
Project description:Cytosine (C) modifications within CpG dyads are central regulatory elements of mammalian genomes. In addition to 5-methylcytosine (mC), genomes can also contain high levels of 5-hydroxymethylcytosine (hmC) that is read differently by nuclear proteins than mC. However, hmC can co-exist with C and mC in different combinations in the two strands of CpG dyads, and it is poorly understood, how these combinatorial marks differ in their protein interactomes and regulatory functions. To identify nuclear binding proteins, we employed DNA promoter probes with differentially modified CpG dyads in pulldown experiments. The datasets comprise three biological replicates of HEK293T nuclear proteins binding to a VEGFA promoter sequence with differentially modified CpG dyads. Each biological replicate contains five technical replicates per modified CpG dyad, resulting in a total of 15 replicates for C/C, mC/mC and hmC/mC, and 10 replicates for hmC/C and hmC/hmC.
2024-08-15 | MSV000095609 | MassIVE
Project description:RNA-seq of TC28a2 cells following TRPV4 activation/inhibition in the presence and absence of prior TGFβ3 stimulation. The experiment was performed to determine the effect of TRPV4 activity on gene expression in the presence and absence of TGFβ stimulation. TGFβ3 was used to stimulate TGFβ signalling, GSK1016790A (GSK101) was used to activate TRPV4, GSK2193874 (GSK219) was used to inhibit TRPV4 and DMSO was used as a vehicle control.
2022-01-17 | E-MTAB-10279 | biostudies-arrayexpress
Project description:Promoter CpG content regulates DNMT-dependent silencing dynamics
| PRJNA930777 | ENA
Project description:Comparing gene expression profile in 3T3-F442A adipocytes with shRNA against TRPV4 or GFP. TRPV4 is an ion channel expressed in adipocytes. Results provided information that how loss-of-function of TRPV4 affects gene expression in adipocytes.
2012-10-12 | GSE40280 | GEO
Project description:The NF-κB signaling pathway plays a critical role in activating macrophages in the pathogenesis of many pro-inflammatory diseases. Mounting evidence has pointed to the importance of tissue mechanical properties in modulating key cellular pro-inflammatory responses. Previous studies have highlighted the role of the mechanosensitive membrane cation channel transient receptor potential vanilloid 4 (TRPV4) in limiting macrophage pro-inflammatory responses and attenuating lung injury in bacterial pneumonia. Our current study demonstrates that alveolar macrophage TRPV4 suppresses pro-inflammatory gene expression following activation of multiple Toll-like receptors (e.g., TLR 1, 2, 4, and 9) in response to P. aeruginosa pneumonia in vivo and TLR agonists in vitro, highlighting the broad regulatory role of TRPV4 in modulating the inflammatory response. TRPV4 suppresses pro-inflammatory cytokines by dampening p65-dependent cytokine transcriptional activity, thereby implicating TRPV4 as a negative regulator of the NF-κB pathway. Upon stimulation with lipopolysaccharide (LPS), TRPV4 translocates to the plasma membrane, in part releasing p65 for nuclear translocation. In addition, TRPV4 was found to have sequence homology with IκBα largely within the TRPV4 ankyrin repeat domain (ANKRD), suggesting that TRPV4 may be acting as a mechanosensitive inhibitor of NF-κB. Further, TRPV4 ANKRD was proven to be critical for TRPV4 binding to the NF-κB pathway subunit, p65, in live cells. Given the diverse roles of TRPV4 and NF-κB/p65 in different cell types, we provide a specific example of novel mechanosensitive crosstalk in macrophages that have general consequences to a broad array of NF-κB dependent inflammatory and malignant diseases.
2025-12-23 | GSE295714 | GEO
Project description:TRPV4 is a cell surface-expressed calcium-permeable cation channel that mediates cell-specific effects on cellular morphology and function. Dominant missense mutations of TRPV4 cause various forms of inherited neuropathy, but the pathogenic mechanisms are unknown. Using an unbiased screen, we sought to identify novel TRPV4 interactors that may be relevant to disease pathogenesis.
2021-01-29 | PXD023758 | Pride
Project description:Effect of how CpG density on the promoter affects the gene silencing and DNA methylation rate of a promoter
2023-03-01 | GSE224403 | GEO