Ontology highlight
ABSTRACT:
PROVIDER: PRJNA753202 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15403581.fastq.gz | Fastqsanger.gz | |||
| SRR15403582.fastq.gz | Fastqsanger.gz | |||
| SRR15403583.fastq.gz | Fastqsanger.gz | |||
| SRR15403584.fastq.gz | Fastqsanger.gz | |||
| SRR15403585.fastq.gz | Fastqsanger.gz |
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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.
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Project description:Simple and efficient delivery of CRISPR genome editing systems in primary cells remains a major challenge. Here, we describe an engineered Peptide-Assisted Genome Editing (PAGE) CRISPR-Cas system for rapid and robust editing of primary cells. PAGE couples a cell-penetrating Cas protein with a cell-penetrating endosomal escape peptide in a 30-minute incubation that yields up to ~98% editing efficiency in primary human and mouse T cells. PAGE provides a broadly generalizable platform for next generation genome engineering in primary cells. CITATION INFORMATION: Zhang Zhen, Baxter Amy E, Ren Diqiu, Qin Kunhua, Chen Zeyu, Collins Sierra M., Huang Hua, Komar Chad A., Bailer Peter F., Parker Jared B., Blobel Gerd A., Kohli Rahul M., Wherry E. John*, Berger Shelley,*, and Shi Junwei*. Peptide-assisted genome editing permits efficient CRISPR engineering of primary T cells.
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2013-09-01 | GSE47455 | GEO
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Project description:Chromogranin A (CHGA) is elevated in plasma of patients with renal failure and several CHGA polymorphisms are associated with hypertensive renal disease. Therefore, we investigated the role of CHGA in kidney disease using the partial nephrectomy model of kidney failure. Mice under surgery to remove 2/3rds of the left kidney and the entire right kidney. Control mice received the sham surgery. Wild-type and CHGA-/- mice used. To model the changes in vitro, CRL-1927 kidney cells were treated with or without CHGA in vitro.
2018-10-25 | GSE106300 | GEO
Project description:Objective: Our study aimed to evaluate differences in plasma lipidome between patients with asymptomatic hyperuricemia (HUA) detected < 40 years (HUA<40) and > 40 years, gout patients with disease onset < 40 years (Gout<40) and > 40 years, and normouricemic healthy controls.
Methods: Plasma samples were collected from 94 asymptomatic HUA (77% HUA<40) subjects, 196 gout patients (59% Gout<40), and 70 normouricemic controls. A comprehensive targeted lipidomic analysis was performed to semi-quantify 608 lipids in plasma. Univariate and multivariate statistics and advanced visualizations were applied.
Results: Both HUA and gout patients showed similar changes in lipid profiles with the highest upregulation of phosphatidylethanolamines (median fold-changes and p-values were 2.9/3.4 and p=1.5x10-16/p=5.5x10-21 for HUA/Gout, respectively) and downregulation of lysophosphatidylcholine plasmalogens/plasmanyls (median fold-changes and p-values were 0.3/0.5 and p=4.8x10-21/p=2.2x10-21 for HUA/Gout, respectively). More profound changes were observed in HUA<40 and Gout<40. Moreover, a shift in the lipid profile towards controls was apparent in HUA<40 and Gout<40 during urate-lowering treatment. Multivariate statistics differentiated HUA<40 and Gout<40 groups from controls with an overall accuracy of > 94%.
Conclusion: The changes in the lipidome of HUA and Gout patients show a significant impact on lipid metabolism and a severe pathobiochemical effect, with no relationship with common determinants such as body mass index, metabolic syndrome, or pathogenic variants in major urate transporter ABCG2. The most significant glycerophospholipid dysregulation was found in HUA<40 and Gout<40 patients, together with a correction of this imbalance with urate-lowering treatment.
2023-03-30 | MSV000091596 | MassIVE