GEO 数据集

主题由标题与摘要自动归类；样本量为数据集标注之和，SuperSeries 可能与其 SubSeries 重复计算。

• NLRP3 inflammasome-mediated pyroptosis exacerbates insulin resistance upon exposure to nanoplastics with different surface chemistries
  GSE338308Danio rerio15 个样本2026-10-31

  The surface chemical properties of nanoplastics (NPs), such as surface charge and functional groups, can markedly influence their toxicological effects. Recent studies have shown that NPs can disrupt glucose homeostasis. However, under metabolically susceptible conditions, such as hyperglycemia and metabolic dysfunction, differences in metabolic toxicity and the underlying mechanisms among surface-modified NPs remain unclea
• Transcriptomic responses of zebrafish following dietary exposure to the short chain PFAS perfluorohexanoic acid (PFHxA)
  GSE291637Danio rerio19 个样本2026-10-31

  Per- and polyfluoroalkyl substances (PFAS) have garnered tremendous concern due to the widespread contamination and environmental persistence as PFAS and their heavy use in commercial products. While the properties of PFAS are useful for various consumer goods, the same properties result in high persistence of PFAS in the environment as well as an increased risk of exposure and deleterious effects for humans and ecosystems. To address data gaps for less studied PFAS, the use of molecular tools is essential to identify novel toxicity pathways that help to reduce additional animal testing for this large chemical class. In our current study, we exposed a model species (zebrafish) to a short chain PFAS, perfluorohexanoic acid (PFHxA), via the diet, which is an understudied exposure route in fish. Fish were exposed over 28 days to a measured low dietary dose (57.6 ng/g) as well as a higher dose (60.7 ng/g). At the end of the exposure, liver tissues were processed for mRNA and libraries were prepared for RNA-seq analysis. In addition to the transcriptome, qPCR will be performed to further assess changes in gene expression due to PFHxA dietary exposure. This study will be the first to examine sub-chronic dietary exposures to PFHxA and the resulting impacts on the transcriptome.
• zebrafish retina m6A epitranscriptome
  GSE186488Danio rerio4 个样本2026-10-31

  m6A epitranscriptome of the retinas of adult zebrafish was sequenced using MeRIP-seq
• SH2 Domain Protein E sustains perivascular fibroblasts to maintain arterial stability
  GSE352057Danio rerio8 个样本2026-10-29

  Developing arteries must withstand pulsatile blood flow while remaining sufficiently flexible to accommodate changing hemodynamic demands. Endothelial interactions with perivascular cells and extracellular matrix are essential for this balance, but the signaling mechanisms that coordinate them remain incompletely understood. We previously showed that SH2 domain protein E (She), an endothelial adaptor protein implicated in ABL signaling, limits the size of the dorsal aorta (DA) in zebrafish embryos. Here, we investigated why zebrafish she mutants subsequently develop DA collapse and circulatory failure at 4–5 days post-fertilization. Before circulatory failure, the mutant DA retained an approximately circular cross-section and showed no detectable changes in the endothelial cell geometry, but exhibited increased distensibility during the cardiac cycle. Mutants had fewer perivascular stromal cells between the DA and posterior cardinal vein, smaller perivascular col1a1 and col5a1 expression domains, and reduced col1a1 transcript level. Single-cell RNA sequencing independently identified a reduced relative abundance of perivascular fibroblast subpopulation. In contrast, DA-associated mural cell numbers, laminin immunoreactivity, and local col4a1 transcript levels were not detectably altered. Ablation of pdgfrb-positive cells largely prevented DA narrowing and circulatory failure, while the nitric oxide donor sodium nitroprusside provided partial rescue. These findings support a contribution of mural cell-dependent vascular tone to collapse of the mechanically vulnerable DA. Mutants also exhibited cardiac chamber enlargement, increased atrial and bulbus arteriosus deformation, atrioventricular regurgitation, and increased Elastin B accumulation in the enlarged bulbus arteriosus. However, endocardial-specific She expression failed to rescue circulatory failure, supporting its requirement in vascular endothelium. Together, these findings link She function to perivascular fibroblast abundance, fibrillar collagen-gene expression, and arterial stability. They support a model in which impaired perivascular support renders the developing DA susceptible to mural cell-associated collapse, extending the role of She from early vessel-size regulation to maintenance of vascular function.

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