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Transcriptomic analysis of HIV-associated nephropathy (Tg26) mouse kidney treated with INT-747 and nicotinamide riboside

ABSTRACT: We analyzed the transcriptomic profiles of Tg26 mouse kidney cortex treated by FXR agonist (INT-747) or by nicotinamide riboside (NR) by bulk mRNA-seq.

ORGANISM(S): Mus musculus

PROVIDER: GSE252711 | GEO | 2025/05/15

REPOSITORIES: GEO

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Transcriptomic analysis of HIV-associated nephropathy (Tg26) mouse kidney treated with INT-747 and nicotinamide riboside

Project description:Transcriptomic analysis of HIV-associated nephropathy (Tg26) mouse kidney treated with INT-747 and nicotinamide riboside

| PRJNA1062305 | ENA

Transcriptomic analysis of HIV-associated nephropathy (Tg26) mouse kidney [bulk RNA-seq]

Project description:We analyzed the transcriptomic profiles of Tg26 mouse kidney cortex by bulk mRNA-seq with or without treatment by PKR inhibitor (C16).

2024-05-27 | GSE205058 | GEO

Transcriptomic analysis of HIV-associated nephropathy (Tg26) mouse kidney [single-nuclear RNA-seq]

Project description:We analyzed the transcriptomic profiles of Tg26 mouse kidney by single-nuclear RNA-seq with or without treatment by PKR inhibitor (C16).

2024-05-27 | GSE205059 | GEO

Gene expression profiling in human precision-cut liver slices upon treatment with the FXR agonist obeticholic acid [human]

Project description:Background: The bile acid-activated farnesoid X receptor (FXR) is a nuclear receptor regulating bile acid, glucose and cholesterol homeostasis. Obeticholic acid (OCA; also known as INT-747 or 6α-ethyl-chenodeoxycholic acid), a promising drug for the treatment of non-alcoholic steatohepatitis (NASH) and type 2 diabetes, activates FXR. Mouse studies demonstrated that FXR activation by OCA (INT-747) alters hepatic expression of many genes. However, no data are available on the effects of OCA in human liver. Here, we generated gene expression profiles in human precision-cut liver slices (hPCLS) after treatment with OCA. Methods: hPCLS were incubated with OCA for 24 h. WT or FXR -/- mice received OCA or vehicle by oral gavage for 7 days. Results: Transcriptomic analysis showed that well-known FXR target genes, including NR0B2 (SHP), ABCB11 (BSEP), SLC51A (OSTα) and SLC51B (OSTβ) and ABCB4 (MDR3), are regulated by OCA in hPCLS. Ingenuity pathway analysis confirmed that 'FXR/RXR activation' is the most significantly changed pathway upon OCA treatment. Comparison of gene expression profiles in hPCLS and mouse livers identified 18 common potential FXR targets. ChIP-sequencing in mouse liver confirmed FXR binding to IR1 sequences of Akap13, Cgnl1, Dyrk3, Pdia5, PPP1R3B and Tbx6. Conclusions: Our study shows that hPCLS respond to OCA treatment by upregulating well-known FXR target genes, demonstrating its suitability to study FXR-mediated gene regulation. We identified 6 novel bona-fide FXR target genes in both mouse and human liver. Finally, we discuss a possible explanation for changes in HDL/LDL observed in NASH and primary biliary cirrhosis patients treated with OCA based on the genomic expression profile in hPCLS.

2016-01-27 | GSE76161 | GEO

Gene expression profiling in human precision-cut liver slices upon treatment with the FXR agonist obeticholic acid [mouse]

2016-01-27 | GSE76162 | GEO

Gene expression profiling and TF occupancy upon treatment with the FXR agonist obeticholic acid

Project description:The farnesoid X receptor (FXR) is a nuclear receptor activated by bile acids and regulates bile acid metabolism, glucose and cholesterol homeostasis. From mouse studies we know that the novel FXR agonist obeticholic acid (OCA) regulates expression of many genes in the liver, but there is currently no data on the effects of OCA on human liver gene expression. This is especially relevant since the novel FXR agonist OCA is currently tested in clinical trials for the treatment of several diseases, such as nonalcoholic steatohepatitis (NASH), nonalcoholic fatty liver disease (NAFLD) and Type 2 Diabetes. In this study we investigate the effect of OCA treatment on gene expression profiles and localization of FXR to the genome in relevant liver samples. ChIP-Seq for FXR in Liver tissue from 2 male mice treated with OCA/INT-747 (10mg/kg/day) and 2 male mice treated with vehicle (1% methyl cellulose).

2016-01-27 | E-GEOD-73624 | biostudies-arrayexpress

Analysis of gene expression in HIV transgenic mice (TG26) with lymphoma in comparison to asymptomatic TG26 mice, and background control (FVBN).Tg26 carries a pNL4-3 HIV-1 provirus lacking part of the gag-pol region, rendering the virus non-infectious.

Project description:About 15% of the TG26 mice develop lymphoma. HIV protein expression is observed, particularly the protein p17/Matrix. Total cellular RNA from spleen and lymph nodes from 3 groups of animals: FVB/N controls (n=3), Tg26 asymptomatic (n=6), and Tg26 with lymphoma (n=6). Results provide insights into the gene expression program in animals with lymphoma.

2016-11-01 | GSE87546 | GEO

Transcriptomic analysis of HIV-associated nephropathy (Tg26) mouse kidney

Project description:Transcriptomic analysis of HIV-associated nephropathy (Tg26) mouse kidney

| PRJNA843463 | ENA

Increased hepatoprotective effects of the novel farnesoid X receptor agonist INT-787 versus obeticholic acid in a mouse model of nonalcoholic steatohepatitis

Project description:We applied RNA sequencing to study the hepatic gene expression profile of Lep(ob/ob) mice fed the Amylin liver NASH (AMLN) diet for 14 weeks and then treated for 2 weeks with vehicle (n=10), obeticholic acid (OCA) (n=9), or INT-787 (n=9). INT-787, which is equipotent to OCA but more hydrophilic, modulated a substantially greater number of genes associated with FXR signaling, lipid metabolism, and stellate cell activation relative to OCA.

2024-04-11 | GSE263273 | GEO

Nicotinamide riboside kinases display redundancy in mediating nicotinamide mononucleotide and nicotinamide riboside metabolism in skeletal muscle cells.

Project description:ObjectiveAugmenting nicotinamide adenine dinucleotide (NAD+) availability may protect skeletal muscle from age-related metabolic decline. Dietary supplementation of NAD+ precursors nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR) appear efficacious in elevating muscle NAD+. Here we sought to identify the pathways skeletal muscle cells utilize to synthesize NAD+ from NMN and NR and provide insight into mechanisms of muscle metabolic homeostasis.MethodsWe exploited expression profiling of muscle NAD+ biosynthetic pathways, single and double nicotinamide riboside kinase 1/2 (NRK1/2) loss-of-function mice, and pharmacological inhibition of muscle NAD+ recycling to evaluate NMN and NR utilization.ResultsSkeletal muscle cells primarily rely on nicotinamide phosphoribosyltransferase (NAMPT), NRK1, and NRK2 for salvage biosynthesis of NAD+. NAMPT inhibition depletes muscle NAD+ availability and can be rescued by NR and NMN as the preferred precursors for elevating muscle cell NAD+ in a pathway that depends on NRK1 and NRK2. Nrk2 knockout mice develop normally and show subtle alterations to their NAD+ metabolome and expression of related genes. NRK1, NRK2, and double KO myotubes revealed redundancy in the NRK dependent metabolism of NR to NAD+. Significantly, these models revealed that NMN supplementation is also dependent upon NRK activity to enhance NAD+ availability.ConclusionsThese results identify skeletal muscle cells as requiring NAMPT to maintain NAD+ availability and reveal that NRK1 and 2 display overlapping function in salvage of exogenous NR and NMN to augment intracellular NAD+ availability.

| S-EPMC5518663 | biostudies-literature

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