The effect of IL-1β on the expression of small RNA in mouse chondrocyte
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE233430 | GEO | 2025/05/01
REPOSITORIES: GEO
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Project description:IL-1B is an important cytokine that is often found to be up-regulated during osteoarthritic and rheumatoid joint diseases. It is viewed as a catabolic factor, inducing enzymes that allow for the degradation of the cartilage extracellular matrix and also has essential roles as an autocrine and paracrine factor in fibronectin fragment-mediated degradation. It can also reduce the synthesis of the major cartilage components, type II collagen and aggrecan. On the other hand, IL-1B also has the ability to induce the growth and morphogenic factor BMP-2. During joint diseases, IL-1B is synthesized by both synovial cells and chondrocytes. Addition of IL-1 biological antagonists such as IL-1 receptor antagonists can suppress cartilage degradation in vitro. Thus, the production of IL-1B could act as the first step in mediating a cascade of other mediators in cartilage which could be relevant to the fate of the cartilage. In order to obtain a global picture of the effect of IL-1B production on human adult articular chondrocytes, we analyzed changes in gene expression induced by IL-1B by microarray analysis. We found that IL-1B has a diverse effect on gene expression profile in chondrocytes. One of the predominant responses that we observed in adult human articular chondrocytes on exposure to IL-1B is a dramatic increase in a large set of chemokines and other genes related to the inflammatory cascade. Keywords: Gene response to IL-1B (10 ng/ml) Cartilage was obtained from adult human tissue donors with above the knee amputations due to chondrosarcoma or traumatic injury or from autopsy. Chondrocytes were isolated following established protocols, maintained in high density, and treated with IL-1B (10 ng/ml). Chondrocytes treated with buffer only served as the untreated control. The experiment was carried out in duplicate. Total RNA was extracted from these chondrocytes, labeled with fluorophores (Cy3 or Cy5) and analyzed for expression changes using the Human Operon/Qiagen v3.0 oligonucleotide array. The analysis was repeated with the fluorophore dyes exchanged between the untreated and experimental RNAs.
2008-05-14 | E-GEOD-11427 | biostudies-arrayexpress
Project description:IL-1B is an important cytokine that is often found to be up-regulated during osteoarthritic and rheumatoid joint diseases. It is viewed as a catabolic factor, inducing enzymes that allow for the degradation of the cartilage extracellular matrix and also has essential roles as an autocrine and paracrine factor in fibronectin fragment-mediated degradation. It can also reduce the synthesis of the major cartilage components, type II collagen and aggrecan. On the other hand, IL-1B also has the ability to induce the growth and morphogenic factor BMP-2. During joint diseases, IL-1B is synthesized by both synovial cells and chondrocytes. Addition of IL-1 biological antagonists such as IL-1 receptor antagonists can suppress cartilage degradation in vitro. Thus, the production of IL-1B could act as the first step in mediating a cascade of other mediators in cartilage which could be relevant to the fate of the cartilage. In order to obtain a global picture of the effect of IL-1B production on human adult articular chondrocytes, we analyzed changes in gene expression induced by IL-1B by microarray analysis. We found that IL-1B has a diverse effect on gene expression profile in chondrocytes. One of the predominant responses that we observed in adult human articular chondrocytes on exposure to IL-1B is a dramatic increase in a large set of chemokines and other genes related to the inflammatory cascade. Keywords: Gene response to IL-1B (10 ng/ml)
2008-05-14 | GSE11427 | GEO
Project description:Although regeneration of human cartilage is inherently inefficient, age is an important risk factor for Osteoarthritis (OA). Recent reports have provided compelling evidence that juvenile chondrocytes (from donors below 13 years of age) are more efficient at generating articular cartilage as compared to adult chondrocytes. However, the molecular basis for such a superior regenerative capability is not understood. In order to identify the cell-intrinsic differences between juvenile and adult cartilage, we have systematically profiled global gene expression changes between a small cohort of human neonatal/juvenile and adult chondrocytes. No such study is available for human chondrocytes although ‘young’ and ‘old’ bovine and equine cartilage have been recently profiled.
2017-09-22 | GSE104113 | GEO
Project description:Inflammation, which is mainly sustained by pro-inflammatory cytokines such as IL-1β, TNF-α, and IL-6, plays an important role in osteoarthritis progression. However, the therapeutic failures of recent clinical trials evaluating anti-IL-1, anti-TNF, and anti-IL-6 drugs highlight the lack of overall understanding of the effects of these cytokines on chondrocytes. Here, we generated a comprehensive transcriptomic and proteomic dataset of osteoarthritic chondrocytes treated with these cytokines to describe their pro-inflammatory signature and compare it to the transcriptome of non-osteoarthritic chondrocytes. We first identified specific dysregulation of metabolic-related genes in OA chondrocytes. A metabolic shift, toward increased glycolysis at the expense of mitochondrial respiration, was specifically identified and confirmed by Seahorse® assay of osteoarthritic chondrocytes treated with IL-1β or TNF-α. These data show a strong association between inflammation and metabolism, indicating that understanding metabolic dysregulations should be a focus of future investigations for the design of therapies for osteoarthritis.
2023-05-20 | GSE215039 | GEO
Project description:The objective was to study the time-course effects of interleukin-1β (IL-1β) on equine articular cartilage, with the aim to identify genes of relevance for cartilage pathology in osteoarthritis. Changes in gene expression related to inflammation, extracellular matrix, and phenotypic alterations was studied.
2018-05-02 | GSE100083 | GEO
Project description:Osteoarthritis is a chronic disease characterised by the loss of articular cartilage in synovial joints through a process of extracellular matrix destruction that is strongly associated with inflammatory stimuli. Chondrocytes undergo changes to their protein translation capacity during osteoarthritis, but a study of how disease-relevant signals effect chondrocyte protein translation at the transcriptomic level has not previously been performed. In this study we describe how the inflammatory cytokine interleukin 1-beta (IL-1β) rapidly affects protein translation in the chondrocytic cell line SW1353. Using ribosome profiling we demonstrate that IL-1β induced altered translation of inflammatory-associated transcripts such as NFKB1, TNFAIP2, MMP13, CCL2 and CCL7, as well as a number of ribosome-associated transcripts, through differential translation and the use of multiple open reading frames. Proteomic analysis of the cellular layer and the conditioned media of these cells identified that proteins which were differentially translated were most readily detected in the secretome. These translationally regulated secreted proteins included a number of chemokines and cytokines, underlining the rapid, translationally-mediated inflammatory cascade that is initiated by IL-1 β.
2019-07-12 | E-MTAB-7466 | biostudies-arrayexpress
Project description:IL-1β promotes the proliferation of rat chondrocytes and inhibits the proliferation of mouse chondrocytes.
2022-02-09 | GSE163080 | GEO
Project description:Long non-coding RNAs (lncRNAs) play pivotal roles in diseases such as osteoarthritis (OA). However, knowledge of the biological roles of lncRNAs is limited in OA. We aimed to explore the biological function and molecular mechanism of HOTTIP in chondrogenesis and cartilage degradation. We used the human mesenchymal stem cell (MSC) model of chondrogenesis, in parallel with, tissue biopsies from normal and OA cartilage to detect HOTTIP, CCL3, and miR-455-3p expression in vitro. Biological interactions between HOTTIP and miR-455-3p were determined by RNA silencing and overexpression in vitro. We evaluated the effect of HOTTIP on chondrogenesis and degeneration, and its regulation of miR-455-3p via competing endogenous RNA (ceRNA). Our in vitro ceRNA findings were further confirmed within animal models in vivo. Mechanisms of ceRNAs were determined by bioinformatic analysis, a luciferase reporter system, RNA pull-down, and RNA immunoprecipitation (RIP) assays. We found reduced miR-455-3p expression and significantly upregulated lncRNA HOTTIP and CCL3 expression in OA cartilage tissues and chondrocytes. The expression of HOTTIP and CCL3 was increased in chondrocytes treated with interleukin-1β (IL-1β) in vitro. Knockdown of HOTTIP promoted cartilage-specific gene expression and suppressed CCL3. Conversely, HOTTIP overexpression reduced cartilage-specific genes and increased CCL3. Notably, HOTTIP negatively regulated miR-455-3p and increased CCL3 levels in human primary chondrocytes. Mechanistic investigations indicated that HOTTIP functioned as ceRNA for miR-455-3p enhanced CCL3 expression. Taken together, the ceRNA regulatory network of HOTTIP/miR-455-3p/CCL3 plays a critical role in OA pathogenesis and suggests HOTTIP is a potential target in OA therapy.
2019-08-12 | PXD014988 | Pride
Project description:Mesenchymal stem cells are often transplanted in inflammatory environments and they are able to survive and modulate host immune responses through mechanism poorly understood. In this paper we analyzed biological responses of MSC in response IL-1β as a representative inflammatory mediator. Microarray analysis of MSC treated with IL-1β revealed that this cytokine activates a set of biological process related with cell survival, cell migration, cell adhesion, chemokine production, induction of angiogenesis and modulation of immune response. Further analysis by real-time PCR and functional assays revealed that IL-1β mainly increases production of chemokines CCL5, CCL20, CXCL1, CXCL3, CXCL5, CXCL6, CXCL10, CXCL11 and CX3CL1, interleukins IL-6, IL-8, IL23A, IL32, Toll-like receptors TLR2, TLR4, CLDN1, metalloproteins MMP1 and MMP3, growth factors CSF2 and TNF, together with adhesion molecules ICAM1 and ICAM4. Functional analysis of MSC proliferation, migration and adhesion to extracellular matrix components revealed that IL-1β did not affect proliferation whereas constitute a throphic factor for MSC and increases adhesion mainly to collagen and laminin. Moreover, IL-1β treatment enhanced the ability of MSC to recruit monocytes and granulocytes cells in vitro. Blockade of NFkβ transcription factor activation with IκB kinase beta (IKKb) siRNA impaired MSC migration, adhesion and leucocyte recruitment, indicating that NF-kB signaling pathway is the main mechanism implicated in these biological processes. These findings are relevant for designing protocols that implicate MSC delivery into inflammatory environments.
2012-06-22 | GSE33755 | GEO
Project description:The effect of IL-1β on the expression of small RNA in mouse chondrocyte
| PRJNA976250 | ENA