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Kidney transcriptome of aged and young wild-type mice (RNA-seq)

ABSTRACT: RNA-sequencing of kidney tissue from aged (28-32 months) and young (3 months) wild-type C57BL/6J mice, used to characterize transcriptional changes associated with natural aging. Kidney was collected for bulk RNA-seq to compare age-related transcriptional changes to those observed with chronic NAD deficiency in ANDY mice fed a niacin-free diet (NFD vs CD; deposited separately as the recovery_kidney SubSeries). This dataset was generated in support of: Benitez-Rosendo, A. & Feuz, M. B. et al. 'Inducible chronic NAD deficiency in mice reveals multi-systemic phenotypical, metabolic, and transcriptional changes.' Nature Communications (in revision; NCOMMS-26-053722-T) (Fig. 6e-h).

ORGANISM(S): Mus musculus

PROVIDER: GSE345593 | GEO | 2026/09/08

REPOSITORIES: GEO

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Project description:Purpose: We examined the impact of niacin on muscle gene expression in mitochondrial myopathy patients and healthy controls. Methods: Muscle transcriptomics profiles were generated using global transcriptomics analysis by RNA sequencing which was performed by the Beijing Genomic Institute (BGI) using their standard protocols Results: The pathway enrichment analysis of RNA-sequencing data indicated that phagosome formation, serine/glycine/one-carbon pathways (de novo serine biosynthesis, purine degradation, glutathione metabolism), LXR/RXR activation, eicosanoid, glycoprotein 6, atherosclerosis, iron homeostasis and cAMP-mediated signalling pathways were among the most significantly changed in patients. Only five and two of the disease associated pathways remained significantly changed after 4- and 10-month supplementation, respectively, in patients as compared to controls. The most prominent niacin-related transcriptomic change in patients’ muscle (patient 10-months on niacin vs patient baseline) was wide-spread downregulation of mTOR-dependent cytoplasmic translation, involving a large number of cytoplasmic ribosome subunits as well as translation initiation factor eIF1. In patients, niacin activated also the peroxisome proliferator-activated receptor signaling pathway, known to induce mitochondrial biogenesis. Niacin also led to decreased atherosclerosis signaling including lowered apolipoprotein expression in patients. The healthy control muscles showed only few changes after 4-months of niacin. To examine in detail the effects of NAD-booster niacin in the mitochondrial integrated stress response (ISRmt), we studied the effects NAD+ boosting for the expression of 24 ISRmt target genes in the patients’ muscle. The analysis confirmed wide-spread induction of these genes, but their expression was unaffected by niacin (ATF5 and its targets ASNS, TRIB3, FGF21, GDF15, MTHFD2, and MTHFD1L; de novo synthesis of serine, PSAT1, PHGDH and SHMT2; glutathione metabolism GPX3 and GSR; and unfolded protein response ER CHOP). Conclusions: These results showed that niacin modulated the expression of disease associated pathways and suppressed mTOR signalling in patients but niacin did not affect disease-related ISRmt signalling.

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Kidney transcriptome of aged and young wild-type mice (RNA-seq)

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