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 |
Items per page: 5 1 - 5 of 24 |
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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.
2008-06-15 | E-GEOD-6979 | biostudies-arrayexpress
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. Keywords: Genetic Modification
2007-11-29 | GSE6979 | GEO
Project description:Rapid increase of fibroblast growth factor 21 under protein malnutrition and its impact on growth and lipid metabolism
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Project description:One of the main regulators of phosphate homeostasis is fibroblast growth factor 23 (FGF23), secreted by osteocytes. The effects of organic versus inorganic dietary phosphate on this homeostasis is unclear. This study used MC3T3-E1 osteocyte-like cells to examine the transcriptomic responses to these phosphates. Most importantly, the expression and secretion of FGF23 was only increased in response to organic phosphate. Gene ontology terms related to a response to environmental change were only enriched in osteocytes treated with organic phosphate while osteocytes treated with inorganic phosphate were enriched for terms associated with regulation of cellular phosphate metabolism. Inhibition of MAPK signaling diminished the response of Fgf23 to organic phosphate, suggesting it activates FGF23. TGF-β signaling inhibition increased Fgf23 expression after the addition of organic phosphate, while the negative TGF-β regulator Skil decreased this response. In summary, the observed differential response of osteocytes to phosphate types may have consequences for phosphate homeostasis.
2024-03-18 | GSE245758 | GEO
Project description:Fibroblast growth factor 9 inhibits remyelination via an off target effect on astrocytes in multiple sclerosis
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Project description:Targeting Fibroblast growth factor-23 (FGF23)-responsive pathways in the control of phosphate and vitamin D metabolism
| PRJNA595932 | ENA
Project description:This data describes the first case of oncogenic osteomalacia due to a plexiform fibrohistiocytic tumor which coincidentally has been found for the first time to induce profound muscle weakness via the overexpression of three phosphatonins which resolved fully upon radical resection of the tumor. Much of the literature suggests that oncogenic osteomalacia is usually caused by a benign mesenchymal tumor secreting fibroblast growth factor subtype-23 (FGF23) but other phosphatonins are rarely implicated.We have previously reported a seemingly typical case of oncogenic osteomalacia. Following curative neoplasm resection, we now report unique molecular characteristics and biology of this tumor never described before. A 25-year-old man had been diagnosed with severe oncogenic osteomalacia that gradually crippled him over 6 years. 68Ga-DOTA-TATE PET-CT scan localized the culprit tumor to his left sole which on resection revealed a plexiform fibrohistiocytic tumor positive for CD34 and CD163 with osteoclast-like giant cells and scattered stromal dendritic cells within the tumor. Circulating FGF23 which was elevated more than 2-folds declined to undetectable levels 24 hours after surgery. Microarray analysis showed over 150-fold upregulation in FGF23, matrix extracellular phosphoglycoprotein (MEPE) and secreted frizzled-related protein subtype 4 (sFRP4) genes which corresponded to the same proteins overexpressed on Western blots
2020-10-30 | GSE160445 | GEO
Project description:Effects of fibroblast growth factors (FGF) on dissociated myelinating cultures
| PRJNA229970 | ENA