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Annexin A3 is necessary for artery-vein alignment in the mouse retinas (RNA-seq analysis of isolated retinal endothelial cells from Anxa3 Tie2-cre mutant mice)

ABSTRACT: Annexin A3 is necessary for artery-vein alignment in the mouse retinas (RNA-seq analysis of isolated retinal endothelial cells from Anxa3 Tie2-cre mutant mice)

PROVIDER: PRJNA559173 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9920770.fastq.gz	Fastqsanger.gz
	SRR9920771.fastq.gz	Fastqsanger.gz
	SRR9920772.fastq.gz	Fastqsanger.gz
	SRR9920767.fastq.gz	Fastqsanger.gz
	SRR9920768.fastq.gz	Fastqsanger.gz

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Annexin A3 is necessary for artery-vein alignment in the mouse retinas (RNA-seq analysis of isolated retinal endothelial cells from Anxa3;Tie2-cre mutant mice)

Project description:Annexin A3 (Anxa3) is a member of the calcium-regulated, cell membrane binding family of Annexin proteins. We previously confirmed that Anxa3 is expressed in the endothelial lineage in vertebrates and that loss of Anxa3 in Xenopus laevis leads to embryonic blood vessel defects. However, the biological function of Anxa3 in mammals is completely unknown. In order to investigate Anxa3 vascular function in mammals, we generated an endothelial cell specific Anxa3 conditional knockout mouse model (Anxa3f/f;Tie2-Cre).

2019-08-08 | GSE135528 | GEO

Annexin A3 is necessary for parallel artery-vein alignment in the mouse retina.

Project description: Not available

| S-EPMC7995330 | biostudies-literature

Tie2+ vs Tie2- macrophages bulk RNAseq

Project description:Tie2+ vs Tie2- macrophages bulk RNAseq

| PRJEB103104 | ENA

Tie2+ vs Tie2- macrophages bulk RNAseq

Project description:BulkRNAseq to identify Tie2+ macrophages signature. Cells were sorted for CD14+ and Tie2 (PTEK). Two fractions were hence sequenced on NextSeq platform (Illumina) after full length cDNA amplification using the SMART-Seq mRNA LP kit (Takara).

2026-03-31 | E-MTAB-15962 | biostudies-arrayexpress

RNA-sequencing of Endothelial Cell Lines Expressing TIE2 WT or Mutant TIE2-L914F

Project description:To investigate the transcriptional effects of venous malformation causative somatic mutation in TIE2 p.L914F mutation on endothelial cells, bulk RNA-sequencing was performed on endothelial cells lines expressing TIE2 wildtype or mutant TIE2-L914F

2025-09-26 | GSE307395 | GEO

miRNA expression profiles of TIE2 expressing Monocytes (TEMs)

Project description:To identify the miRNA expressing profiles of TIE2 expressing Monocytes (TEMs), we have employed the Agilent Human miRNA 8×60K (Design ID:046064) microarray. Human peripheral blood mononuclear cells (PBMCs) in venous blood from healthy donors were isolated by Lymphoprep (Axis-Shield, Norway). Human monocytes in PBMCs, identified as cells that expressed CD14, were enriched by positive immunomagnetic selection using anti-CD14 MicroBeads (Miltenyi, Germany). TEMs (TIE2+CD14+) and TIE2-Monocytes (Tie2-CD14+) were then isolated by FACS-sorting (Aria II, BD Biosciences) using FITC-conjugated anti-CD14 (BD Biosciences, USA) and APC-conjugated anti-TIE2 (R&D System, USA) antibodies.Three TEMs samples together with their paried TIE2-Monocytes were detected.

2017-05-19 | GSE68322 | GEO

Annexin 10 promotes invasion in QBC-939 cell

Project description:Annexin family is the largest category of eukaryotic calcium and phospholipid-binding proteins and plays important roles in various physiological processes, including cell differentiation and proliferation. More than 160 Annexin proteins are classified into 65 different speciesAs a new member of Annexin family, the role of ANXA10 in cancer progression is rarely investigated, and its expression and function in CCA need more experiments to reveal.

2022-05-17 | GSE132279 | GEO

Gene expression profiles of TIE2 expressing Monocytes (TEMs)

Project description:To identify the gene expressing profiles of TIE2 expressing Monocytes(TEMs), we have employed the Agilent lncRNA Gene Expression 4Ã180K(Design ID:042818) microarray. Human peripheral blood mononuclear cells (PBMCs) in venous blood from healthy donors were isolated by Lymphoprep (Axis-Shield, Norway). Human monocytes in PBMCs, identified as cells that expressed CD14, were enriched by positive immunomagnetic selection using anti-CD14 MicroBeads (Miltenyi, Germany). TEMs (TIE2+CD14+) and TIE2-Monocytes (Tie2-CD14+) were then isolated by FACS-sorting (Aria II, BD Biosciences) using FITC-conjugated anti-CD14 (BD Biosciences, USA) and APC-conjugated anti-TIE2 (R&D System, USA) antibodies.Three TEMs samples together with their paried TIE2-Monocytes were detected.Expressions of sixteen genes (CDKN1A, FDXR, SESN1, BBC3 and PHPT1) from this signature was quantified in the same RNA samples by real-time PCR, confirming low variability between donors as well as the predicted radiation response pattern. The gene expressions of three independent paried TEMs and TIE2- Monocytes samples from different donors were measured.

2017-05-17 | E-GEOD-57783 | biostudies-arrayexpress

Role of annexin A2 in muscle repair

Project description:Repair of injured muscle involves repair of injured myofibers through the involvement of dysferlin and its interacting partners, including annexin. Studies with mice and patients have established that dysferlin deficit leads to chronic inflammation and adipogenic replacement of the diseased muscle. However, longitudinal analysis of annexin deficit on muscle pathology and function is lacking. Here we show that unlike annexin A1, but similar to dysferlin, lack of annexin A2 (AnxA2) causes poor myofiber repair and progressive weakening with age. However, unlike dysferlin-deficient muscle, AnxA2-deficient muscles do not exhibit chronic inflammation or adipogenic replacement. Deletion of AnxA2 in dysferlin deficient mice reduces inflammation, adipogenic replacement, and loss in muscle function caused by dysferlin deficit. These results show that: a) AnxA2 facilitates myofiber repair, b) chronic inflammation and adipogenic replacement of dysferlinopathic muscle requires AnxA2, and c) inhibiting AnxA2-mediated inflammation is a novel therapeutic avenue for dysferlinopathy.

2016-10-04 | GSE87557 | GEO

Annexin A1 exerts renoprotective effects in experimental crescentic glomerulonephritis

Project description:The glucocorticoid-inducible protein annexin A1 has been shown to function as key-regulator of the resolution phase of inflammation but its role in immune-mediated crescentic glomerulonephritis has not been studied so far. Acute crescentic glomerulonephritis was induced in annexin A1 deficient and wildtype mice using a sheep serum against rat glomerular basement membrane constituents. Alterations in gene expression were determined by RNA-Seq and gene ontology analysis. Intrinsic annexin A1 has a protective effect in reducing pro-inflammatory signals and infiltration of neutrophil granulocytes during crescentic GN. The annexin A1 signaling cascade may therefore provide novel targets for the treatment of inflammatory kidney disease.

2022-10-04 | GSE204873 | GEO

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