Global gene expression profiles were compared among IL1B-treated, Ad-OSCAR-treated, and control mice, with or without subsequent treatment with OSCAR inhibitors (Brivudine or Adefovir).
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE298720 | GEO | 2026/05/30
REPOSITORIES: GEO
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Project description:To examine the effects of Oscar and its inhibitor 5-ASA on articular cartilage, we established OSCAR overexpressed chondrocytes with adenovirus and treated 5-ASA subsequently. Gene expression profiling analysis was performed using articular cartilage transcriptomes, with biologic replicates, generated by RNA-seq.
2023-06-30 | GSE207056 | GEO
Project description:Purpose: RNA sequencing (RNA-Seq) analyses of articular cartilage obtained after DMM surgery in Oscar-/- and WT mice. The purpose of this experiment was to demonstrate how the deficiency of Oscar gene affects downstream signal transduction in articular cartilage. Methods: Articular cartilage mRNA profiles of 10-weeks-old wild-type (WT) and Oscar knockout (Oscar−/−) mice were performed for the destabilization of the medial meniscus (DMM) and each cartilage tissue sample was harvested from two time-points (2- and 4-weeks after surgery). Sequencing libraries were prepared according to the manufacturer’s instructions (TruSeq Stranded mRNA Library Prep Kit; Illumina, San Diego, CA, USA). Paired-end sequencing of 101-mer read length was performed using a HISEQ 2500 sequencing system (Illumina). The sequencing quality of raw FASTQ files was assessed using FastQC (https://www.bioinformatics.babraham.ac.uk/projects/fastqc/). Low-quality reads and adapter sequences in reads were eliminated using BBDuk (http://jgi.doe.gov/data-and-tools/bb-tools/). Results: Usinig RNA-Seq data in articular cartilage tissues from WT and Oscar–/– mice subjected to sham or DMM surgery and each cartilage sample obtained from 2- and 4-week time points after surgery, respectively. And we found that significantly enriched pathways in the 1270 common genes. Conclusions: Our study represents the Oscar gene deficiency analysis of articular cartilage transcriptomes, with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. Our results show that NGS offers a comprehensive and more accurate quantitative and qualitative evaluation of mRNA content within a cell or tissue. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions.
2020-03-26 | GSE147529 | GEO
Project description:Inflammation is characterized by a biphasic cycle consisting initially of a pro-inflammatory phase which is subsequently resolved by anti-inflammatory processes. The coordination of these two disparate states needs to be highly controlled, suggesting that the regulation of the cytokines that drive these processes are intimately linked. Interleukin-1 beta (IL1B) is a master regulator of pro-inflammation and is encoded within the same topologically associated domain (TAD) as interleukin-37 (IL37). IL37 has recently emerged as a powerful anti-inflammatory cytokine which diametrically opposes the function of IL1B. Within this TAD, we identified a novel long non-coding RNA called AMANZI which negatively regulates IL1B expression and trained immunity through the induction of IL37 transcription. We found that the activation of IL37 occurs through the formation of a dynamic long-range chromatin contact that leads to the temporal delay of anti-inflammatory responses. The common variant rs16944 present in AMANZI augments this regulatory circuit, predisposing individuals to enhanced pro-inflammation or immunosuppression. Our work illuminates a chromatin-mediated biphasic circuit coordinating expression of IL1B and IL37, thereby regulating two functionally opposed states of inflammation from within a single TAD.
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Project description:To identify genes that maintain the homeostasis of the articular cartilage, we compared gene expression profiles of adult articular cartilage chondrocytes with that of growth plate cartilage chondrocytes in adult (10-week-old) Sprague Dawley (SD) rats. Furthermore, to identify genes that have a potency to regenerate the articular cartilage, we compared gene expression profiles of superficial layer chondrocytes of infant epiphyseal cartilage which form articular cartilage with that of the deep layer chondrocytes which form growth plate cartilage in infant (6-day-old) SD rats.
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2011-09-30 | E-GEOD-29233 | biostudies-arrayexpress
Project description:To examine the unbiased global gene expression of over-expression of Prg4 in superficial zone articular chondrocytes in mice. This approach allows us to define novel signaling changes caused by the over-expression of Prg4 in superficial zone articular chondrocytes Total RNA was isolated from superficial zone chondrocytes in P1 articular cartilage in hind limbs (n=3) by laser capture microdissection. Same tissue from wild type mice served as control
2013-06-24 | E-GEOD-43663 | biostudies-arrayexpress
Project description:To understand the effect of semaphorin 4D on articular chondrocytes, articular chondrocytes were stimulated with semaphorin 4D. Total RNA was analyzed by RNA-seq.
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Project description:This network was obtained by combining (with an OR logical operator) the following list of IL1B_secretion activators:
TXNIP AND IL1B - reference in pubmed:23747245
IL1B AND hydrogen_peroxide - reference in pubmed:20023662
NLRP3_PYCARD_CASP1_complex AND IL1B AND cholesterol_crystal - reference in pubmed:23747245
IL1B AND NLRP3 AND hydrogen_peroxide - reference in pubmed:20023662
IL1B AND oxLDL AND TLR4 - reference in pubmed:23812099
IL1B AND glucose - reference in pubmed:20023662
IL1B AND IL1B_secretion - reference in pubmed:23747245
IL1B AND CASP8 - reference in pubmed:22365665
NLRP3_PYCARD_CASP1_complex AND NFE2L2 AND IL1B - reference in pubmed:23747245
PYCARD AND IL1B AND hydrogen_peroxide - reference in pubmed:20023662
IL1B AND NLRP3 AND glucose - reference in pubmed:20023662
NFE2L2 AND IL1B - reference in pubmed:23747245
IL1B AND mitochondrial_respiratory_chain_complex_I - reference in pubmed:21124315
TXNIP AND IL1B AND glucose - reference in pubmed:20023662
IL1B AND oxLDL AND CD36 - reference in pubmed:23812099
IL1B AND ripoptosome - reference in pubmed:22365665
NLRP3_PYCARD_CASP1_complex AND IL1B - reference in pubmed:23747245
2018-11-16 | MODEL1712240002 | BioModels
Project description:Osteoarthritis (OA) is the most common form of arthritis worldwide. It is a complex disease affecting the whole joint but is generally characterized by progressive degradation of articular cartilage. Recent genome-wide association screens have implicated distinct DNA methylation signatures in OA patients. We show that the de novo DNA methyltransferase (Dnmt) 3b, but not Dnmt3a, is present in healthy murine and human articular chondrocytes and expression decreases in OA mouse models and in chondrocytes from human OA patients. Targeted deletion of Dnmt3b in murine articular chondrocytes results in an early onset and progressive post-natal OA-like pathology. RNA-seq and MethylC-seq analyses of Dnmt3b loss-of-function chondrocytes shows that cellular metabolic processes are affected. Specifically, TCA metabolites and mitochondrial respiration are elevated. Importantly, a chondroprotective effect was found following Dnmt3b gain-of-function in murine articular chondrocytes in vitro and in vivo. This study shows that Dnmt3b plays a significant role in regulating post-natal articular cartilage homeostasis. Cellular pathways regulated by Dnmt3b in chondrocytes may provide novel targets for therapeutic approaches to treat OA.
2017-07-24 | GSE85148 | GEO
Project description:We identify pathways regulated by IL1b/TNFa ICV injection and EAE in astrocytes
2020-02-12 | GSE137314 | GEO