Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA985630 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25010030_1.fastq.gz | Fastqsanger.gz | |||
| SRR25010030_2.fastq.gz | Fastqsanger.gz | |||
| SRR25010031_1.fastq.gz | Fastqsanger.gz | |||
| SRR25010031_2.fastq.gz | Fastqsanger.gz | |||
| SRR25010032_1.fastq.gz | Fastqsanger.gz |
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Project description:Fibroblast growth factor-23 (FGF23) is a bone-derived hormone that has recently received much attention due to its association with the progression of chronic kidney disease, cardiovascular disease, and associated mortality. Extracellular sodium ion concentration ([Na+]) plays a significant role in bone metabolism. Both hyponatremia (low serum [Na+]) and hypernatremia (high serum [Na+]) have been shown to affect bone remodeling. However, nothing is known about the impact of [Na+] on FGF23 production. Here, we show that elevated [Na+] (by +20 mM) suppressed FGF23 formation, whereas low [Na+] (by -20 mM) led to an increase in FGF23 synthesis in the osteoblast-like cell line UMR-106. Similar bidirectional changes in FGF23 were observed when osmolality was altered by mannitol but not by urea, suggesting a role of tonicity in FGF23 formation. Moreover, these changes in FGF23 were inversely proportional to the expression of NFAT5 (nuclear factor of activated T cells-5), a transcription factor responsible for tonicity-mediated cellular adaptations. On the other hand, arginine vasopressin (AVP), which is often responsible for hyponatremia, did not affect FGF23 production. Next, comprehensive and unbiased RNA-seq analysis of UMR-106 cells exposed to low vs. high [Na+] revealed several novel genes involved in cellular adaptation to altered tonicity. Additional analysis of cells with Crisp-Cas9 mediated NFAT5 deletion indicated that NFAT5 controls numerous genes associated with FGF23 synthesis, thereby confirming its role in [Na+]-mediated FGF23 regulation. In line with these findings, in a pilot study, we found that human hyponatremic patients have higher FGF23 levels. Our results suggest that [Na+] is a critical regulator of FGF23 synthesis.
2023-06-23 | GSE235694 | GEO
Project description:Fibroblast growth factor 23 (FGF23) is a member of endocrine FGF subfamily, which includes FGF19, FGF21 and FGF23. We explored the question of whether different FGF ligands are activating the same transcriptional program in prostate cancer (PCa) cells or whether there are unique or partially overlapping activities as well.
2015-05-29 | GSE62192 | GEO
Project description:Fibroblast growth factor-23 (FGF23), a circulating protein produced in bone, causes renal inorganic phosphate (Pi) wasting by down-regulation of sodium phosphate co-transporter 2a (Npt2a). The mechanism behind this action is unknown. We have previously generated transgenic mice (TG) expressing human wild-type FGF23 under the control of the α1 (I) collagen promoter. In this study we performed a large scale gene expression study of kidneys from TG mice and wild-type littermates. Several genes that play a role in Pi regulation had decreased expression levels, such as Npt2a, but also Pdzk1 which is a scaffolding protein known to interact with NPT2a. Importantly, the Klotho gene, a suggested crucial co-factor for FGF23 receptor binding and activation, was the most affected decreased gene. However, other genes proposed to regulate Pi levels, such as secreted Frizzled Related Protein 4 (sFRP4), Na+/H+ exchanger regulatory factor 1 (NHERF1) and the FGF-receptors 1-4, revealed no changes. Interestingly, expression levels of inflammatory response genes were increased and histological analysis revealed tubular nephropathy in the TG mice kidneys. In conclusion, FGF23 TG mice have altered kidney gene expression levels of several genes thought to be part of Pi homeostasis and an increase in inflammatory response genes, data supported by histological analysis. These findings may lead to further understanding of how FGF23 mediates its actions on renal Pi regulation. Experiment Overall Design: Five kidneys from FGF23 TG mice and five kidneys from WT littermates was used for Affymetrix Genechip analysis. One Genechip was used/animal. Animals were 8 weeks old when kidneys were collected.
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Project description:Rattus norvegicus Fgf23, fibroblast growth factor 23 [Source:RGD Symbol;Acc:620178], is differentially expressed in 21 experiment(s);
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Project description:Rattus norvegicus Fgf23, fibroblast growth factor 23 [Source:RGD Symbol;Acc:620178], is expressed in 2 baseline experiment(s);
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