Danio rerio
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA382561 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5443710.fastq.gz | Fastqsanger.gz | |||
| SRR5443711.fastq.gz | Fastqsanger.gz | |||
| SRR5443712.fastq.gz | Fastqsanger.gz | |||
| SRR5443713.fastq.gz | Fastqsanger.gz | |||
| SRR5443704.fastq.gz | Fastqsanger.gz |
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Project description:Here, we performed single nuclear RNA-seq (snRNA-seq) of control and Pitx2 deficient cardiac tissue 3 weeks post myocardial infarction. Next, unsupervised graph-based clustering of the combined snRNA-Seq data set mapped to both introns and exons, comprising 7848 cells. Overall, we identified nine transcriptionally distinct clusters representing all the major cardiac cell types, including cardiac fibroblasts (FB), cardiomyocytes (CM), endothelial cells (EC), vascular smooth muscle cells (SMC), macrophages (Mφ), epicardial cells (EpiC), endocardial cells (EndoC), lymphatic endothelial cells (LEC), and mural cells or pericytes (PeC). Moreover, two distinct populations of fibroblasts, designated FB-1 and FB-2, were also identified.
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Project description:The meningeal lymphatic network—housed within the dural meninges surrounding the brain— is critical for cerebrospinal fluid (CSF) drainage. Through continuous brain interstitial fluid (ISF) mixing with CSF via the glymphatic system, this lymphatic network facilitates the removal of central nervous system (CNS) waste. During aging and in Alzheimer’s disease (AD), attenuated meningeal lymphatic drainage promotes the buildup of toxic misfolded proteins—including amyloid beta—in the CNS. Alleviating this age-related meningeal lymphatic dysfunction represents a promising therapeutic strategy to alleviate AD pathology. However, the mechanisms underlying this lymphatic decline remain elusive. Here we demonstrate that age-related alterations in meningeal immunity contribute to meningeal lymphatic impairment. Single-cell RNA-sequencing of dural lymphatic endothelial cells in aged mice demonstrated a response signature to the cytokine IFNγ, which was elevated in the aged dura due to meningeal T cell accumulation. Chronic elevation of IFNγ in the meninges of young mice via AAV-mediated overexpression altered lymphatic adherans junctions and impaired CSF drainage to deep cervical lymph nodes—comparable to the deficits observed in aged mice. Direct disruption of lymphatic junctions via CSF-delivered VE-Cadherin disrupting antibodies was sufficient to phenocopy impairments in CSF drainage. Therapeutically, IFNγ neutralization in aged mice alleviated age-related impairments in meningeal lymphatic function. These data suggest manipulation of meningeal immunity as a viable therapeutic target to normalize CSF drainage in aged mice and alleviate the pathology in AD mice associated with impaired waste removal.
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