Inflammatory response to IL-1b in WT, LDHA KO, NAMPT KO, NFKBIZ KO and FX11 treated chondrocytes
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PROVIDER: PRJNA623356 | ENA |
REPOSITORIES: ENA
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Project description:Our goal is to study the impacts of IL-1b treatment on chondrocyte physiology. Furthermore, we knocked out several genes that we believe are important for modulating the inflammatory response. We find that IL-1b treatment induces metabolic reprogramming towards aerobic glycoylsis. We found that inhibition of LDHA using inbhitiro FX11 inhibited the inflammatory response of chondrocytes. We hypothesized that this effect was mediated by interaction with NADH, leading to regulation of IkB-z protein. Thus, deletion of LDHA, NAMPT or NFKBIZ was performed and found to inhibit inflammatory response genes induced by IL-1b, with similar gene expression changes amongst the three suggesting that they may work in the same pathway.
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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.
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Project description:To survey altered gene expreesion in round, colmnar and hypertrophic chondrocytes of Tric-b-KO mice, total RNA preparations from round chondrocytes and colmnar/hypertrophic chondrocytes were subjected to gene microarray analysis. Results provide insight into the transcriptional profile of each Tric-b-KO chondrocyte and provide further insight into their functions.
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Project description:ARID1B KO in liver leads to minimal gene expression changes, whereas ARID1A/1B DKO leads to global gene expression changes.
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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)
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Project description:To elucidate the function of AP-1B in small intestinal epithelia, which is well known as one of the components of the AP-1 clathrin adaptor complex, gene expression profiling of AP-1B KO mice was performed.
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Project description:To elucidate the function of AP-1B in small intestinal epithelia, which is well known as one of the components of the AP-1 clathrin adaptor complex, gene expression profiling of AP-1B KO mice was performed. Small intestine of AP-1B +/- and -/- mice were dissected and soaked in Hank's Buffered Salt Solution (HBSS) (GIBCO) containing 30 mM EDTA. After incubation on ice for 20 min, IECs were isolated by manipulation with a fine needle under stereomicroscopic monitoring (n=2).
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Project description:Neural stem/progenitor cell (NSPC) proliferation and self-renewal, as well as insult-induced differentiation, decrease markedly with age, but the molecular mechanisms responsible for these declines remain unclear. Here we show that levels of NAD+ and nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme in mammalian NAD+ biosynthesis, decrease with age in the hippocampus. Ablation of Nampt in adult NSPCs reduced their pool and proliferation in vivo. The decrease in the NSPC pool during aging can be rescued by enhancing hippocampal NAD+ levels. Nampt is the main source of NSPC NAD+ levels and required for G1/S progression of the NSPC cell cycle. Nampt is also critical for oligodendrocytic lineage fate decisions through a mechanism mediated redundantly by Sirt1 and Sirt2. Ablation of Nampt in the adult NSPCs in vivo reduced NSPC-mediated oligodendrogenesis upon injury. These phenotypes recapitulate defects in NSPCs during aging, implicating Nampt-mediated NAD+ biosynthesis as a mediator of these age-associated functional declines. Total RNA obtained from neurospheres derived from postnatal hippocampi subjected to 48 hours in vitro of incubation with Nampt-specific inhibitor FK866 (10 nM, 4 samples) or vehicle (DMSO, 1:1000, 4 samples).
2014-05-08 | E-GEOD-49784 | biostudies-arrayexpress
Project description:NAMPT is an enzyme in the mammalian NAD+ salvage pathway. Expression microarray analysis was used to study the effect of NAMPT knockdown on gene expression in MCF-7 breast cancer cells. Experiment Overall Design: Stable knockdown of NAMPT was achieved using a retroviral shRNA construct. An shRNA directed against Luciferase was used to generate the Luc control cells. Three independent biological replicates with matching Luc controls were analyzed using Affymetrix U133 A2.0 microarrays.
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Project description:To investigate the function of Myl3 in in primary chondrocytes, we generated Col2a1-Cre: Myl3fl/fl (Myl3-KO) conditional knockout mice.We then performed RNA sequencing analysis with primary chondrocytes from Myl3-KO or control mice.
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