The RNA-seq for the kidneys injected with cisplatin and NAD precursors.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE207587 | GEO | 2023/02/03
REPOSITORIES: GEO
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Project description:The RNA-seq for the kidneys injected with cisplatin and NAD precursors.
| PRJNA856281 | ENA
Project description:Here, we performed proteomics of kidneys obtained from patients with obstructive nephropathy and healthy controls (n=11/8), or from unilateral ureteral obstruction (UUO) mice and sham mice (n=6/6). Proteomic measurement of all human kidney samples resulted in a total of 6089 proteins with an average of 5780 proteins per sample. Compared to control kidneys, 614 proteins were up-regulated and 855 proteins were down-regulated (p value < 0.05, q value < 0.05, and fold change > 2 or < 0.5) in human obstructed kidneys. The up-regulated proteins were significantly enriched in collagen formation and immune response. Moreover, the human and mouse kidney proteomics reveled an aberrant NAD+ metabolism and NAD+-related metabolic pathways, including mitochondrial dysfunction, oxidative phosphorylation, and tryptophan metabolism. The expression patterns of several key enzymes catalyzing NAD+ biosynthesis and consumption were dramatically altered in obstructive nephropathy. Moreover, the major NAD+ consumer CD38 was strongly induced in obstructed kidneys which contributed to the decline of renal NAD+ levels. Functional studies demonstrated that CD38 deletion or inhibition significantly recovered renal NAD+ levels and reduced obstruction-induced renal fibrosis.
2023-01-08 | PXD039314 |
Project description:Friedreich’s ataxia (FRDA) is a progressive disorder caused by insufficient expression of frataxin, which plays a critical role in assembly of iron-sulfur centers in mitochondria. Individuals are cognitively normal, but display a loss of motor coordination and cardiac abnormalities. Many ultimately succumb to heart failure. Administration of nicotinamide adenine dinucleotide (NAD+) precursors has shown promise in mitochondrial myopathy and rodent models of heart failure, including mice lacking frataxin in cardiomyocytes. We studied mice with systemic knockdown of frataxin (shFxn), which display motor deficits and early mortality with cardiac hypertrophy. Hearts in these mice do not “fail” per se but become hyperdynamic with small chamber sizes. Data from an ongoing natural history study indicate that hyperdynamic hearts are observed in young individuals with FRDA, suggesting that the mouse model could reflect early pathology. Administering nicotinamide mononucleotide or riboside to shFxn mice increases survival, modestly improves cardiac hypertrophy, and limits increases in ejection fraction. Mechanistically, most of the transcriptional and metabolic changes induced by frataxin knockdown are insensitive to NAD+ precursor administration, but glutathione levels are increased suggesting improved antioxidant capacity. Overall, our findings indicate that NAD+ precursors are modestly cardioprotective in this model of Friedreich’s Ataxia and warrant further investigation.
2024-08-28 | GSE271798 | GEO
Project description:These are the raw mass spec data files for manuscript "NAD precursors cycle between host tissues and the gut microbiome", Karthikeyani Chellappa et al. Check out "Mass Spec data_KEY_Chellappa et al Cell Metabolism_2022.xlsx" for data file arrangement.
2022-10-06 | MSV000090481 | MassIVE
Project description:Supplemental NAD+ precursors show metabolic and functional benefits in rodent models of disease and are being explored as potential therapeutics in human studies. However, the wide range of processes that involve NAD+ in every cell and subcellular compartment make it difficult to narrow down mechanisms of action. Here we provide evidence that for a well-established benefit of NAD+ precursors in mice, faster liver regeneration, nearly the entire effect can be attributed to the concentration of NAD+ in hepatocyte mitochondria. We find that mitochondrial NAD+ concentration in hepatocytes of male mice is determined by the expression of the transporter SLC25A51 (MCART1), as has previously been shown in cultured cells. Heterozygous loss of SLC25A51 modestly decreases mitochondrial NAD+ content in multiple tissues and impairs liver regeneration, while hepatocyte-specific overexpression is sufficient to enhance regeneration comparably to the effect of systemic supplements, despite increasing NAD+ only in mitochondria. Thus, the hepatocyte mitochondrial NAD+ pool is a key determinant of the rate of liver regeneration.
2025-11-06 | PXD067549 | Pride
Project description:Expression data from Stx2-injected (i.p.) mouse kidneys
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Project description:NAD+ levels decline with age and in certain disease conditions. NAD+ precursors have been shown to stimulate NAD+ biosynthesis and ameliorate various age-associated diseases in mouse models. However, NAD+ metabolism is complicated in cancer and its role in triple-negative breast cancer (TNBC) remains elusive. Here, we show that NAD+ supplement suppresses tumor metastasis in a TNBC orthotopic patient-derived xenograft (PDX) model. Sirtuin1 lysine deacetylase (SIRT1) is required for the effects since SIRT1 knockdown blocks NAD+-suppressed tumor metastasis. Overexpression of SIRT1 effectively impairs the metastatic potential of TNBC. Importantly, the interaction between SIRT1 and p66Shc causes the deacetylation and functional inactivation of p66Shc, which inhibits epithelial-mesenchymal transition (EMT). Overall, we demonstrate that NAD+ supplementation executes its anti-tumor function via activating the SIRT1-p66Shc axis, which highlights the preventive and therapeutic potential of SIRT1 activators as effective interventions for TNBC.
2023-01-23 | GSE220683 | GEO
Project description:The goal of this project is to obtain the expression pattern of miRNAs in wild type kidneys at various ages during development. The data is obtained from mouse kidneys of ages P0, P7, P14, P21 and P35. The analysis compares the expression levels of miRNAs between the age groups.
2022-07-19 | GSE208429 | GEO
Project description:In the present study we applied NAD captureSeq to charecterize the 5'-NAD-RNA profile of E. coli BW25113 wt strain as well as nudC and csdA knockouts. The data obtained showed that both knockouts resulted in an increased number of identified 5’-NAD-RNA species, thus suggesting that CsdA might add a potentially new layer of control on NAD-epitranscriptomic landscape.
2023-08-22 | GSE224605 | GEO
Project description:Supplemental NAD+ precursors show metabolic and functional benefits in rodent models of disease and are being explored as potential therapeutics in human studies. However, the wide range of processes that involve NAD+ in every cell and subcellular compartment make it difficult to narrow down mechanisms of action. Here we provide evidence that for a well-established benefit of NAD+ precursors in mice, faster liver regeneration, nearly the entire effect can be attributed to the concentration of NAD+ in hepatocyte mitochondria. We find that mitochondrial NAD+ concentration in hepatocytes of male mice is determined by the expression of the transporter SLC25A51 (MCART1), as has previously been shown in cultured cells. Heterozygous loss of SLC25A51 modestly decreases mitochondrial NAD+ content in multiple tissues and impairs liver regeneration, while hepatocyte-specific overexpression is sufficient to enhance regeneration comparably to the effect of systemic supplements, despite increasing NAD+ only in mitochondria. Thus, the hepatocyte mitochondrial NAD+ pool is a key determinant of the rate of liver regeneration.
2025-08-15 | MSV000098839 | MassIVE