Small RNA-Seq of miR-181 deficient Treg cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA512620 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The interdependence of selective cues during development of regulatory T (Treg) cells in the thymus and their suppressive function remains incompletely understood. Here we analyzed this interdependence by taking advantage of highly dynamic changes of miR-181a/b-1 during late T-cell development with very high levels of expression during thymocyte selection followed by massive downregulation in the periphery. Loss of miR-181a/b-1 resulted in inefficient de novo generation of Treg cells in the thymus, but simultaneiously permitted homeostatic expansion in the periphery in the absence of competition. Modulation of T-cell receptor (TCR) signal strength in vivo indicated that miR-181a/b-1 controlled Treg cell formation via establishing adequate signaling thresholds. Unexpectedly, miR-181a/b-1-deficient Treg cells displayed elevated suppressive capacity in vivo, in line with elevated levels of CTLA-4 protein, but not mRNA, in thymic and peripheral Treg cells. Therefore, we propose that intrathymic miR-181a/b-1 controls development of Treg cells and imposes a developmental legacy on their peripheral function.
2019-01-04 | GSE124594 | GEO
Project description:We found miR-125a was a key regulator that stabilizes the commitment and immunoregulatory capacity of Treg cells.To gain insights into the general functional features of miR-125a-deficient Treg cells, we performed a genome-wide gene array analysis on Treg population isolated from the spleens of 6 to 8-week-old miR-125a-deficient and WT mice We sorted CD4+CD25hi Treg population from the spleens of 6 to 8-week-old miR-125a-deficient and their littermate WT mice. Cells were collected and total RNA was extracted for Affymetrix GeneChip®Mouse Genome 430 2.0 Array
2015-05-08 | E-GEOD-66608 | biostudies-arrayexpress
Project description:Expression profiling of miR-142 deficient Treg cells
| PRJNA786239 | ENA
Project description:We found miR-125a was a key regulator that stabilizes the commitment and immunoregulatory capacity of Treg cells.To gain insights into the general functional features of miR-125a-deficient Treg cells, we performed a genome-wide gene array analysis on Treg population isolated from the spleens of 6 to 8-week-old miR-125a-deficient and WT mice
2015-05-08 | GSE66608 | GEO
Project description:The intestinal epithelium is a key physical interface that integrates dietary and microbial signals to regulate nutrient uptake and mucosal homeostasis. Intestinal epithelial cells (IECs) have a high turnover rate driven by the death of terminally differentiated cells with concurrent stem cell proliferation, a process critical for maintaining intestinal homeostasis and protecting against mucosal inflammation. The transcriptional programs that regulate IEC quiescence, proliferation, and differentiation have been well-characterized. However, how gene expression networks critical for IEC functions are regulated at the post-transcriptional level during homeostasis or inflammatory disease remains poorly understood. Herein, we show that a conserved family of microRNAs, miR-181, is significantly downregulated in IECs from patients with inflammatory bowel disease and mice with chemical-induced colitis. Strikingly, we showed that miR-181 expression within IECs, but not the hematopoietic system, is required for protection against the development of severe colonic inflammation in response to epithelial injury in mice. Mechanistically, we showed that miR-181 expression increases the proliferative capacity of IECs, likely through the regulation of Wnt signaling, independently of gut microbiota composition. As epithelial reconstitution is crucial for restoring intestinal homeostasis after injury, the miR-181 family represents a potential novel therapeutic target in IECs for protection against severe intestinal inflammation.
2022-07-25 | GSE208410 | GEO
Project description:miR-181 regulates colonic inflammation
| PRJNA859816 | ENA
Project description:Parkinson’s disease (PD) is caused by loss of dopaminergic (DA) neurons in the substantia nigra (SN). Although PD pathogenesis is not fully understood, studies implicate perturbations in gene regulation, mitochondrial function, and neuronal activity. MicroRNAs (miRs) are small gene regulatory RNAs that inhibit diverse subsets of target mRNAs, and several studies have noted miR expression alterations in PD brains. For example, miR-181a is abundant in brain and is increased in PD patient brain samples; however, the disease relevance of this remains unclear. Herein, we show that miR-181 target mRNAs are broadly down-regulated in aging and PD brains. To address if the miR‑181 family plays a role in PD pathogenesis, we generated adeno-associated viruses (AAV) to overexpress and inhibit miR-181 isoforms. After co-injection with AAV overexpressing alpha-synuclein (aSyn) into mouse SN (PD model), we found that moderate miR-181a/b overexpression exacerbated aSyn-induced DA neuronal loss, whereas miR‑181 inhibition was neuroprotective, relative to controls (GFP-alone and/or scrambled RNA). Also, prolonged miR-181 overexpression in SN alone elicited measurable neurotoxicity coincident with an increased immune response. RNA-seq analyses revealed that miR-181a/b inhibits genes involved in synaptic transmission, neurite outgrowth, and mitochondrial respiration, along with several genes having known protective roles and genetic links in PD.
2022-03-23 | GSE196441 | GEO
Project description:Analysis of HeLa cells at 24 hours after transfection with wild type miR-1, miR-124, miR-181 versus control transfected HeLa cells. Results were compared to protein down-regulation at 48 hours measured by SILAC-MS. Analysis of HeLa cells at 24 hours after transfection with wild type miR-1, miR-124, miR-181 versus control transfected HeLa cells. Results were compared to protein down-regulation at 48 hours measured by SILAC-MS.
2010-05-25 | E-GEOD-11968 | biostudies-arrayexpress
Project description:Study designed to determine the immediate effects of supplementing OSK reprogramming with miR-294 or miR-181. MEFs were infected on day 0, and transfected with miR-294, miR-181 or control mimic on day 1. On day 3 RNA was extracted. OSK infected MEFs samples were compared to non-infected MEFs and to fully reprogrammed iPSCs.
2013-09-15 | GSE49556 | GEO
Project description:Analysis of HeLa cells at 24 hours after transfection with wild type miR-1, miR-124, miR-181 versus control transfected HeLa cells. Results were compared to protein down-regulation at 48 hours measured by SILAC-MS.
2008-07-31 | GSE11968 | GEO