Bi-directional interactions of omental adipocytes and SKOV3ip1 cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA986819 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Primary human omental adipocytes were isolated from patients with non-cancer conditions. Subsequently, gene expression profiled in adipocytes and ovarian cancer cell line (SKOV3ip1) alone (control) or under co-culture conditions. Following co-culture cells were separated and total RNA isolated for microarray analysis.
2023-07-24 | GSE235641 | GEO
Project description:Modifiable hydrogels have revealed tremendous insight into how physical characteristics of cells’ 3D environment drive stem cell lineage specification. However, in native tissues, cells do not passively receive signals from their niche. Instead they actively probe and modify their pericellular space to suit their needs, yet the dynamics of cells’ reciprocal interactions with their pericellular matrix when encapsulated within hydrogels remains relatively unexplored. Here, we show that human bone marrow stromal cells (hMSC) encapsulated within hyaluronic acid-based hydrogels modify their pericellular environment through degradation and/or protein secretion, imparting them with similar pericellular stiffnesses, regardless of initial hydrogel properties. These cell-secreted pericellular matrices play a role in regulating hMSC fate, with secretion of a stiff proteinaceous pericellular matrix associated with adipogenesis, and degradation with osteogenesis. Our observations suggest that hMSC participate in a bi-directional interplay between the properties of their 3D milieu and their own secreted pericellular matrix, and that this combination of interactions drives fate.
2018-11-23 | PXD009500 | Pride
Project description:Antisense transcripts play an important role in generating regulatory non-coding RNAs but if these transcripts are also translated and for what purpose is yet poorly understood. Isolation of polysome fractions followed by RNA sequencing and mass spectrometry analysis of a six frame data-base revealed nascent peptides originating from different reading frames of bi-directional transcripts. Two peptides originating from the antisense strand stimulated the proliferation of CD8+ T cells when presented to peripheral blood mononuclear cells (PBMCs) from nine healthy donors. An antigenic peptide derived from the reverse strand of two cDNA constructs was presented on MHC-I molecules and induced CD8+ T cell activation. These results demonstrate that three frame translation of bi-directional transcripts generate antigenic peptide substrates for the immune system. This discovery holds significance for better understanding the origin of self-discriminating peptide substrates for the MHC-I pathway and for enhancing immune-based therapies against infected or transformed cells.
2025-05-07 | PXD057573 | Pride
Project description:Emerging studies reveal that neuropeptides play critical role in regulating anti-helminth immune responses, hinting at the potential of intrinsic enteric neurons (iENs) in orchestrating intestinal immunity. However, whether and how the iENs get activated during infection, and whether they engage in a bi-directional communication with the immune cells, remain poorly defined. Here we show that iENs became activated in response to helminth infection. Single-nucleus RNA sequencing of the iENs revealed significant alterations in gene expression in IL-13R+ intrinsic primary afferent neurons (IPANs), including the upregulation of the neuropeptide -CGRP. Using genetic mouse models, we demonstrated that both group 2 innate lymphoid cells (ILC2s) and neuronal IL-13R signaling are indispensable for optimal iEN activation, which subsequently inhibit ILC2 responses and anti-helminth immunity. Together, these results reveal a previously unrecognized bi-directional neuro-immune crosstalk in the intestine.
2025-01-31 | GSE260708 | GEO
Project description:Circadian rhythms are daily physiological and behavioral changes governed by an internal molecular clock, and dysfunctions in circadian rhythms have long been associated with various neurodegenerative diseases. Abnormal sleep-wake cycle often precedes the onset of cognitive and motor symptoms in patients, while the pathological changes may further exacerbate the disturbance in circadian cycle. It is unclear whether dysregulated circadian rhythm is a consequence of, or a contributing factor for, neurodegeneration. In addition, the evidence directly connecting the neurodegeneration-associated proteins to core circadian clock gene expression remains sparse. Here we show that FUS, a RNA-binding protein implicated in the pathogenesis of ALS and frontotemporal dementia, exhibits a bi-directional regulation with circadian rhythm. Our meta-analysis of RNAseq datasets and subsequent biochemical analysis revealed FUS as a gene regulated by circadian oscillation. Furthermore, NR1D1 binds the FUS promoter and regulates the amplitude of FUS oscillation. Meanwhile, FUS is recruited by transcriptional co-repressor PSF, and is found in the same complex as Bmal-Clock to repress Per2 expression. More strikingly, in cells and brain tissues from homozygous knock-in rats, the pathogenic R521C mutant FUS significantly alters the oscillation patterns of core circadian genes even at young age. Therefore, our results have revealed a novel bi-directional mechanism whereby dysregulated circadian clock and FUS expression may exacerbate neurodegeneration via mutual influence.
2017-04-12 | GSE77572 | GEO
Project description:Idiopathic pulmonary fibrosis (IPF) is the prototypic progressive fibrotic lung disease with a median survival of 2-4 years. Injury to and/or dysfunction of alveolar epithelium are strongly implicated in IPF disease initiation, but what factors determine why fibrosis progresses rather than normal tissue repair occurs remain poorly understood. We previously demonstrated that ZEB1-mediated epithelial-mesenchymal transition (EMT) in human alveolar epithelial type II (ATII) cells augments TGF-β-induced profibrogenic responses in underlying lung fibroblasts by paracrine signalling. Here we investigated bi-directional epithelial-mesenchymal crosstalk and its potential to drive fibrosis progression. RNA sequencing (RNA-seq) of lung fibroblasts exposed to conditioned media from ATII cells undergoing RAS-induced EMT identified many differentially expressed genes including those involved in cell migration and extracellular matrix (ECM) regulation. We confirmed that paracrine signalling between AS-activated ATII cells and fibroblasts augmented fibroblast recruitment and demonstrated that this involved a ZEB1-tissue plasminogen activator (tPA) axis. In a reciprocal fashion, paracrine signalling from TGF-β-activated lung fibroblasts or IPF fibroblasts induced RAS activation in ATII cells, at least partially via the secreted protein, SPARC. Together these data identify that aberrant bi-directional epithelial-mesenchymal crosstalk in IPF drives a chronic feedback loop that maintains a wound-healing phenotype and provides self-sustaining pro-fibrotic signals.
2021-08-19 | PXD025821 | Pride
Project description:Barcoded viral tracing identifies bi-directional immunosuppressive astrocyte-glioblastoma cross-talk
| PRJNA1210635 | ENA
Project description:Bi-directional neuro-immune communication regulates host defense against helminth infection
| PRJNA1082736 | ENA
Project description:Bi-directional ribosome scanning controls the stringency of start codon selection
| PRJNA734658 | ENA
Project description:The cellular mechanisms by which PPARγ improves metabolism in mature human adipocytes and potential depot differences in its actions are poorly understood. To assess the global effects of PPARγ activation on human omental gene expression, we conducted microarray analysis of control vs. rosiglitazone-treated omental tissues from human subjects.
2019-04-30 | GSE122721 | GEO