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Screening of genes differentiating transcriptional profiles of CIA rats at different NAMPT expression statuses

ABSTRACT: Screening of genes differentiating transcriptional profiles of CIA rats at different NAMPT expression statuses

PROVIDER: PRJNA792510 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17334041_1.fastq.gz	Fastqsanger.gz
	SRR17334041_2.fastq.gz	Fastqsanger.gz
	SRR17334042_1.fastq.gz	Fastqsanger.gz
	SRR17334042_2.fastq.gz	Fastqsanger.gz
	SRR17334043_1.fastq.gz	Fastqsanger.gz

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Screening of genes differentiating transcriptional profiles of CIA rats at different NAMPT expression statuses

Project description:We screened out differentially expressed genes between CIA rats and healthy controls at both NAMPT++ (CIA1) and NAMPT+ (CIA2) statuses.It was obvious that that high expression of NAMPT is linked to acute inflammation, as TLRs and its downstream MAPKs and NF-κB were identified as the most affected pathways in NAMPT++ samples compared with normal control. However, by the decrease of NAMPT expression, the pathological situation was not eased but became even more complicated. Energy metabolism (mainly lipid metabolism) was significantly altered at this status. Interestingly, many RA-related pathways emerged, such as TGF-β, IL-17, PI3K-AKT and osteoclast differentiation pathways. These results solidly support the hypothesis that NAMPT overexpression is an early event in CIA and directly affects the innate rather than adaptive immunity.

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Project description:The molecular basis to autoimmune arthritis is unclear. Collagen Induced Arthritis (CIA) in mice, is a model that has many features that resemble Rheumatoid Arthritis (RA), although it does not perfectly duplicate RA. The study of CIA has provided insight into relevant pathogenesis and has aided in the identification of potential therapeutic targets. In this study we used Mouse Cytokine Expression Arrays to examine gene expression levels in joints at early, peak and decline stages during disease in DBA/1 mice. The aim of the study was to identify candidate molecules that may be involved in the development and progression of collagen-induced arthritis (CIA). Keywords: Disease State Analysis

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Project description:Nicotinamide phosphoribosyltransferase (NAMPT) functions in NAD synthesis, apoptosis, and inflammation. Dysregulation of NAMPT has been associated with several inflammatory diseases, including rheumatoid arthritis (RA). The purpose of this study was to investigate NAMPT’s role in arthritis using mouse and cellular models. Collagen-induced arthritis (CIA) in DBA/1J Nampt+/- mice was evaluated by ELISA, micro-CT and RNA-sequencing (RNA-seq). In vitro Nampt loss-of-function and gain-of-function studies on osteoclastogenesis were examined by TRAP staining, nascent RNA capture, luciferase reporter assays, and ChIP-PCR. Nampt-deficient mice presented with suppressed inflammatory bone destruction and disease progression in a CIA mouse model. Nampt expression was required for the epigenetic regulation of the Nfatc1 promoter and osteoclastogenesis. Finally, RNA-seq identified 690 differentially expressed genes in whole ankle joints which associated (P<0.05) with Nampt expression and CIA. Selected target was validated by RT-PCR or functional characterization. We have provided evidence that NAMPT functions as a genetic risk factor and a potential therapeutic target to RA.

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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).

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