Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Bulk RNA-seq of microglia from Apoa1 KO mice injected with ApoA-I protein intravenously

ABSTRACT: Bulk RNA-seq of microglia from Apoa1 KO mice injected with ApoA-I protein intravenously

PROVIDER: PRJNA1101003 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR28710664.fastq.gz	Fastqsanger.gz
	SRR28710665.fastq.gz	Fastqsanger.gz
	SRR28710666.fastq.gz	Fastqsanger.gz
	SRR28710667.fastq.gz	Fastqsanger.gz
	SRR28710668.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 32

Similar Datasets

Bulk RNA-seq of microglia from Apoa1 KO mice injected with ApoA-I protein intravenously

Project description:We found ApoA-I from blood can be taken up by microglia in the brain. To determine if ApoA-I from circulation is sufficient to restore microglial transcriptomic state to a more wild-type-like state, we performed a rescue experiment by intravenously injecting ApoA-I protein into adult Apoa1 KO mice and sorted microglia with or without ApoA-I uptake for bulk transcriptomic analysis.

2024-10-15 | GSE264111 | GEO

Bulk RNA-seq of primary microglia with LPS stress and ApoA-I treatment

Project description:To test the functional role of ApoA-I on microglia in the context of stress, we treated primary microglia with LPS stress with or without ApoA-I protein, and used bulk RNA-seq to evaluate if ApoA-I exhibits an anti-inflammatory role.

2024-10-15 | GSE264110 | GEO

Single cell gene expression profile of bronchoalveolar lavage fluid (BALF) cells from Apoa1-/- and Apoa1+/+ mice challenged with LPS and house dust mite

Project description:Neutrophils play important roles in inflammatory airway diseases. Here, we assessed whether apolipoprotein A-I (apoA-I) modifies neutrophil heterogeneity as part of the mechanism by which it attenuates acute airway inflammation. Neutrophilic airway inflammation was induced by daily intranasal administration of LPS plus house dust mite (LPS+HDM) to Apoa1-/- and Apoa1+/+ mice for 3 days. Single cell RNA sequencing was performed on cells recovered in bronchoalveolar lavage fluid (BALF) on day 4. Unsupervised profiling identified 10 clusters of neutrophils in BALF from Apoa1-/- and Apoa1+/+ mice. LPS+HDM-challenged Apoa1-/- mice had an increased proportion of the Neu4 neutrophil cluster that expressed S100a8, S100a9, and Mmp8, and had high maturation, aggregation, and TLR4 binding scores. There was also an increase in the Neu6 cluster of immature neutrophils, whereas neutrophil clusters expressing interferon-stimulated genes were decreased. An unsupervised trajectory analysis showed that Neu4 represented a distinct lineage in Apoa1-/- mice. LPS+HDM-challenged Apoa1-/- mice also had an increased proportion of recruited airspace macrophages, which was associated with a reciprocal reduction in resident airspace macrophages. Increased expression of a common set of pro-inflammatory genes, S100a8, S100a9, and Lcn2, was present in all neutrophils and airspace macrophages from LPS+HDM-challenged Apoa1-/- mice. Apoa1-/- mice have increases in specific neutrophil and macrophage clusters in the lung during acute inflammation mediated by LPS+HDM, as well as enhanced expression of a common set of pro-inflammatory genes. This suggests that modifications in neutrophil and macrophage heterogeneity contribute to the mechanism by which apoA-I attenuates acute airway inflammation.

2024-07-29 | GSE234287 | GEO

The apoA-I induced transcriptome and dependence on MyD88

Project description:Apolipoprotein A-I is well known to play a role in cholesterol efflux, but our studies suggest that apoA-I may also induce proinflammatory signaling. The molecular mechanisms behind apoA-I-mediated proinflammatory signaling have not yet been explored, nor has the link between this signaling and cholesterol efflux. We hypothesize that apoA-I is a novel TLR agonist, signaling through the MyD88 proinflammatory signaling adaptor to induce cytokines. Microarray analysis confirmed that a suite of pro-inflammatory genes are induced by apoA-I with varying dependence upon MyD88, and that MyD88 regulates >6% of the apoA-I-induced transcriptome.

2010-06-15 | GSE13772 | GEO

N39 APOA1-tdTomato drug screen

Project description:N39 APOA1-tdTomato drug screen

| PRJNA1142560 | ENA

Bulk RNA-seq of primary microglia with LPS stress and ApoA-I treatment

Project description:Bulk RNA-seq of primary microglia with LPS stress and ApoA-I treatment

| PRJNA1101004 | ENA

Transcription profiling of mouse knockouts vs wild type apoE knockout,apoA1 knockout, apoA1 transgene, apoB knockout, mice were fed normal vs artherogenic diets

Project description:Collect tissues from control C57kBL/6 and the following genetically engineered mice-apoE knockout,apoA1 knockout, apoA1 transgene, apoB knockout, LDLR knockout.Both male and female mice fed chow or atherogenic diet will be used. Animals from each group were pooled into 2 pools, one containing 4 mice and the other containing 5 mice

2010-10-10 | E-TIGR-110 | biostudies-arrayexpress

Apoa1, a safe harbor locus for therapeutic genome editing in the liver

Project description:Clinical application of somatic genome editing requires therapeutics that are generalizable to a broad range of patients. Targeted insertion of promoterless transgenes can ensure that edits are permanent, broadly applicable, while minimizing risks of off-target integration. In the liver, the Albumin locus is currently the only well characterized site for promoterless transgene insertion. Using an unbiased ChIP-seq approach, we here identify Apolipoprotein a1 (Apoa1) as one of the most highly expressed and accessible loci in mouse and human liver. We target the Apoa1 locus with Adeno-Associated Viral (AAV) delivery of CRISPR/Cas9, and achieve rates of 6 to 16% with no evidence of toxicity. We further show that the endogenous Apoa1 promoter can drive robust and sustained expression of therapeutic proteins such as factor IX (FIX) or apolipoprotein E (APOE). Finally, we demonstrate that Apoa1-targeted fumarylacetoacetate hydrolase (FAH) can correct and rescue the severe metabolic liver disease hereditary tyrosinemia type I. In summary, we identify and validate Apoa1 as novel safe harbor site for genome editing therapeutics.

2021-06-01 | GSE152993 | GEO

RNAseq data from FACS-sorted microglia from mouse brain from control mice (uninjected) or LPS-injected mice in the context of A20 knockout

Project description:Using RNAseq, we compared the mRNA profiles of microglia in wild type or microglia-specific A20 knockout mice. These mice were either untreated or intraperitoneally injected with LPS (3.5 mg/kg).

2018-07-03 | GSE97538 | GEO

Evaluation of cellular distribution of intravenously injected LNP in the skeletal muscle

Project description:Evaluation of cellular distribution of intravenously injected LNP in the skeletal muscle

| PRJNA1260241 | ENA