Ontology highlight
ABSTRACT:
PROVIDER: PRJNA970661 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24476302_1.fastq.gz | Fastqsanger.gz | |||
| SRR24476302_2.fastq.gz | Fastqsanger.gz | |||
| SRR24476303_1.fastq.gz | Fastqsanger.gz | |||
| SRR24476303_2.fastq.gz | Fastqsanger.gz | |||
| SRR24476304_1.fastq.gz | Fastqsanger.gz |
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Project description:Natural flavonoid pectolinarigenin (PEC) was reported to alleviate tubulointerstitial fibrosis of unilateral ureteral obstruction (UUO) mice in our previous study. To further investigate nephroprotective effects of PEC in hyperuricemic nephropathy (HN), adenine and potassium oxonate induced HN mice and uric acid-treated mouse kidney epithelial (TCMK-1) cells were employed in the study. As a result, PEC significantly lowered serum uric acid level and restored hyperuricemia-related kidney injury in HN mice. Meanwhile, PEC alleviated inflammation, fibrosis and reduced adipokine FABP4 content in the kidneys of HN mice and uric acid-treated TCMK-1 cells. Mechanistically, PEC inhibited the TGF-β1 expression as well as the phosphorylation of transcription factor SMAD3 and STAT3 to regulate the corresponding inflammatory and fibrotic gene expression in kidney tissues. In conclusion, our results suggested that PEC could inhibit the activation of SMAD3 and STAT3 signaling to suppress inflammation and fibrosis, thereby alleviate HN in mice.
2022-02-18 | GSE190205 | GEO
Project description:Aim of the study This study aimed to evaluate the therapeutic efficacy of XZSWD against HUA-induced kidney injury and to elucidate the molecular pathways involved. Methods UPLC-QTOF/MS was used to identify compounds in XZSWD and medicated serum. A HUA mouse model was induced by potassium oxonate (PO) and hypoxanthine (HX) to evaluate the therapeutic effects of XZSWD on renal injury. RNA-Seq and CIBERSORT were applied to analyze gene expression and immune infiltration. Key signaling pathways were validated by qRT-PCR, Western blot, immunofluorescence, and flow cytometry. A THP-1/HK-2 co-culture system combined with SPP1 overexpression and knockdown was used to explore the molecular mechanisms underlying XZSWD’s anti-inflammatory and anti-fibrotic effects. Results 99 compounds were identified in XZSWDS. XZSWD reduced serum uric acid, improved renal function, and suppressed inflammation in HUA mice. RNA-Seq and CIBERSORT revealed downregulation of macrophage-related genes and enhanced mixed M1/M2 polarization. XZSWD inhibited the SPP1–CD44 axis and SRC/FAK/β-Catenin signaling, reducing Epithelial–Mesenchymal Transition (EMT) and Extracellular Matrix (ECM) deposition. In vitro, XZSWD suppressed uric acid-induced EMT and macrophage migration, polarization; these effects were reversed by SPP1 overexpression and enhanced by SPP1 knockdown, indicating SPP1 as a critical therapeutic target. Conclusions The XZSWD alleviates hyperuricemia-induced renal injury by effectively suppressing macrophage-mediated inflammation through coordinated regulation of the SPP1–CD44 axis and the SRC/FAK/β-Catenin signaling network.
2025-07-01 | GSE300922 | GEO
Project description:Katsuwonus pelamis isolate:Western Pacific Genome sequencing
| PRJNA1137481 | ENA
Project description:The effect of uric acid on islet function remains to be confirmed,We applied GSIS, immunofluorescence staining, WB, and flow cytometry to observe the protective effects of uric acid on beta cell apoptosis and insulin deficiency.To further explore the molecular mechanisms involved in this,we found UA could directly suppressed GSIS in both INS-1E cells and primary isolated islets in a dose- and time-dependent manner. RNAseq suggested that CHOP/NLRP3 is critical in the UA-induced beta cell dysfunction. These data suggest that UA might be an independent risk factor for beta cell function which induced beta cell dysfunction via OAT2/chop/ NLRP3 pathway. which provided new insight into the diabetogenic effect of UA.
2025-02-01 | GSE197089 | GEO
Project description:Microarray analysis reveals up-regulation of retinoic acid and hepatocyte growth factor related signaling pathways by pro-insulin C-peptide in kidney proximal tubular cells: Antagonism of the pro-fibrotic effects of TGF-b1 Novel signaling roles for C-peptide have recently been discovered with evidence that it can ameliorate complications of type 1 diabetes. Here we sought to identify new pathways regulated by C-peptide of relevance to the pathophysiology of diabetic nephropathy. Microarray analysis was performed to identify genes regulated by either C-peptide and/or transforming growth factor beta 1 (TGF-β1) in a human proximal tubular cell line, HK-2. Expression of retinoic acid receptor β (RARβ), hepatcoyte growth factor (HGF), cellular retinoic acid binding protein II (CRABPII), vimentin, E-cadherin, Snail and β-catenin was assessed by immunoblotting. The cellular localisation of vimentin and β-catenin was determined by immunocytochemistry. Changes in cell morphology were assessed by phase contrast microscopy. Gene expression profiling demonstrated differential expression of 953 and 1,458 genes after C-peptide exposure for 18h or 48h respectively. From these, members of the anti-fibrotic retinoic acid (RA) and HGF signaling pathways were selected. Immunoblotting demonstrated that C-peptide increased RARβ, CRABPII and HGF. We confirmed a role for RA in reversal of TGF-β1-induced changes associated with epithelial-mesenchymal transition (EMT), including expression changes in Snail, E-cadherin, vimetin and redistribution of β-catenin. Importantly, these TGF-β1-induced changes were inhibited by C-peptide. Further, effects of TGF-β1 on Snail and E-cadherin expression were blocked by HGF and inhibitory effects of C-peptide were removed by blockade of HGF activity. This study identifies a novel role for HGF as an effector of C-peptide, possibly via an RA signaling pathway, highlighting C-peptide as a potential therapy for diabetic nephropathy.
2010-02-11 | GSE20247 | GEO
Project description:Preconditioning strategies like caloric restriction (CR) and hypoxic preconditioning (HP) show remarkable protective effects in animal models of acute kidney injury (AKI). Since the underlying molecular effects are still not fully understood we performed an experiment directly comparing CR and HP in a murine model of ischemia-reperfusion injury (IRI) of the kidney. 8 to 12-week-old, male C57BL6/J mice were either put to 4 weeks of caloric restriction (70% of normal food intake) or placed in a hypoxic chamber (8%O2) for 3 consecutive days prior to IRI. Whole kidneys were used for transcriptional analysis (RNAseq) before and after ischemia-reperfusion injury to look for common effects of both modes of preconditioning.
2019-12-31 | E-MTAB-7982 | biostudies-arrayexpress
Project description:Accumulating evidence suggests the pathogenic role of immunity and metabolism in diabetic kidney disease (DKD). Herein, we aimed to investigate the effect of complement factor B (CFB) on lipid metabolism in the development of DKD. We found that in patients with diabetic nephropathy (DN), the staining of Bb, CFB, C3a, C5a, and C5b-9 were significantly elevated in renal tubulointerstitium. Cfb knockout diabetic mice had significantly milder tubulointerstitial injury and less ceramide biosynthesis. The in vitro study demonstrated that cytokine secretion, endoplasmic reticulum stress, oxidative stress, and cell apoptosis were ameliorated in siCFB HK-2 cells under high glucose conditions. Exogenous ceramide supplementation attenuated the protective effect of CFB knockdown in HK-2 cells, while inhibiting ceramide synthases (CERS) with fumonisin B1 in CFB-overexpressing cells rescued the cell injury. CFB knockdown could downregulate the expression of NF-κB p65, which initiates the transcription of CERS3. Furthermore, C3 knockdown abolished CFB-mediated cytokine secretion, NF-κB signaling activation, and subsequently ceramide biosynthesis. Thus, CFB deficiency inhibited activation of the complement alternative pathway and attenuated kidney damage in DKD, especially tubulointerstitial injury, via inhibiting the NF-κB signaling pathway, further blocking the transcription of CERS, which regulates the biosynthesis of ceramide. CFB may be a promising therapeutic target of DKD.
2023-02-01 | GSE217153 | GEO
Project description:Approximately 15% of US adults have circulating levels of uric acid above its solubility limit, which is causally linked to the inflammatory disease gout. In most mammals, uric acid elimination is facilitated by the enzyme uricase. However, human uricase is a pseudogene, having been inactivated early in hominid evolution. Though it has long been known that a substantial amount of uric acid is eliminated in the gut, the role of the gut microbiota in hyperuricemia has not been studied. Here we identify a gene cluster, widely distributed in the gut microbiome, that encodes a pathway for uric acid degradation. Stable isotope tracing demonstrates that gut bacteria metabolize uric acid to xanthine or short chain fatty acids such as acetate, lactate and butyrate. Ablation of the microbiota in uricase-deficient mice causes profound hyperuricemia, and anaerobe-targeted antibiotics increase the risk of gout in humans. These data reveal a role for the gut microbiota in uric acid excretion and highlight the potential for microbiome-targeted therapeutics in hyperuricemia.
2023-06-16 | GSE206419 | GEO