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Annexin A1 exerts renoprotective effects in experimental crescentic glomerulonephritis

ABSTRACT: Annexin A1 exerts renoprotective effects in experimental crescentic glomerulonephritis

PROVIDER: PRJNA842654 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19415800.fastq.gz	Fastqsanger.gz
	SRR19415801.fastq.gz	Fastqsanger.gz
	SRR19415802.fastq.gz	Fastqsanger.gz
	SRR19415803.fastq.gz	Fastqsanger.gz
	SRR19415804.fastq.gz	Fastqsanger.gz

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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

Annexin A1 exerts renoprotective effects in experimental crescentic glomerulonephritis.

Project description:Non-resolving inflammation plays a critical role during the transition from renal injury towards end-stage renal disease. The glucocorticoid-inducible protein annexin A1 has been shown to function as key regulator in the resolution phase of inflammation, but its role in immune-mediated crescentic glomerulonephritis has not been studied so far. Methods: Acute crescentic glomerulonephritis was induced in annexin A1-deficient and wildtype mice using a sheep serum against rat glomerular basement membrane constituents. Animals were sacrificed at d5 and d10 after nephritis induction. Renal leukocyte abundance was studied by immunofluorescence and flow cytometry. Alterations in gene expression were determined by RNA-Seq and gene ontology analysis. Renal levels of eicosanoids and related lipid products were measured using lipid mass spectrometry. Results: Histological analysis revealed an increased number of sclerotic glomeruli and aggravated tubulointerstitial damage in the kidneys of annexin A1-deficient mice compared to the wildtype controls. Flow cytometry analysis confirmed an increased number of CD45+ leukocytes and neutrophil granulocytes in the absence of annexin A1. Lipid mass spectrometry showed elevated levels of prostaglandins PGE2 and PGD2 and reduced levels of antiinflammatory epoxydocosapentaenoic acid regioisomers. RNA-Seq with subsequent gene ontology analysis revealed induction of gene products related to leukocyte activation and chemotaxis as well as regulation of cytokine production and secretion. Conclusion: Intrinsic annexin A1 reduces proinflammatory signals and infiltration of neutrophil granulocytes and thereby protects the kidney during crescentic glomerulonephritis. The annexin A1 signaling cascade may therefore provide novel targets for the treatment of inflammatory kidney disease.

| S-EPMC9605209 | biostudies-literature

Single-cell TCR-sequencing of T cells in crescentic glomerulonephritis

Project description:Single-cell TCR sequencing of T cells from ANCA-associated glomerulonephritis patients and experimental crescentic glomerulonephritis mouse model.

2023-03-31 | GSE223107 | GEO

Expression data from Annexin A1 Ac1-25 vs. Unstimulated human peripheral blood monocytes

2007-09-19 | GSE9080 | GEO

CC chemokine ligand 18 (CCL18) is associated with disease activity and relapse in ANCA-associated crescentic glomerulonephritis

Project description:Anti neutrophil cytoplasmic antibody (ANCA) associated vasculitis is the most frequent cause of crescentic glomerulonephritis. Histopathologic features and clinical course of the disease are diverse and judgment of disease activity is often limited due to the lack of reliable activity markers. In order to define potentially new molecular or cellular markers in the kidney which may predict clinical outcome, we performed microarray analyses of renal biopsies from patients with ANCA-associated crescentic glomerulonephritis. We correlated expression profiles with clinical data from our prospective study of patients with renal ANCA disease. The CC chemokine ligand 18 (CCL18) was one of the most up-regulated proteins in kidneys of patients with ANCA-associated crescentic glomerulonephritis. CCL18 producing cells in the kidneys were identified as CD68 and CD209 positive myeloid dendritic cells. The density of CCL18 positive cells correlated with the severity of acute tubular injury and with the impairment of renal function. CCL18 protein levels were elevated in serum samples of patients with renal ANCA disease when compared with patients with non- ANCA-associated crescentic glomerulonephritis. Persistence of high CCL18 serum levels correlated with impairment of renal function and the risk of relapsing disease. Therefore, CCL18 might serve as a marker for persistent disease activity and renal relapses in ANCA-associated vasculitis.

2015-09-03 | E-MTAB-1944 | biostudies-arrayexpress

LncRNA Gm26917 promotes macrophage differentiation by enhancing Annexin A1 ubiquitination in LPS-induced acute liver injury

Project description:Our studies demonstrated that Gm26917 localized in the cytoplasm of hepatic macrophages and globally regulated expressions of inflammatory genes and differentiation of macrophages. In vivo study showed that lentivirus-mediated gene silencing of Gm26917 attenuated liver inflammation and protected mice from LPS-induced ALI. Furthermore, mechanistic study showed that 3’- truncation of Gm26917 interacts with N-terminus of Annexin A1, a negative regulator of NF-κB signaling pathway. We also found that Gm26917 knockdown suppressed NF-κB activity by decreasing the ubiquitination of Annexin A1 and its interaction with NEMO. Besides, expression of Gm26917 in inflammatory macrophage was regulated by transcription factor forkhead box M1 (FOXM1). LPS treatment could dramatically increase the binding of FOXM1 to the promoter region of Gm26917 in macrophages. In sum, our findings suggest that lncRNA Gm26917 silencing protected against LPS-induced liver injury by regulating TLR4/NF-κB signaling pathway in macrophages.

2022-09-01 | GSE185716 | GEO

Transcription profiling by array of rat macrophages from WKY/NCrl and LEW/Crl strains to determine susceptibility to glomerulonephritis

Project description:The Wistar-Kyoto (WKY) rat shows marked susceptibility to crescentic glomerulonephritis, while Lewis rats are resistant. Glomerular injury and crescent formation are macrophage-dependent. The aim of this study is to use gene expression profiling to identify genetic factors that determine macrophage activation and render WKY rats susceptibile to glomerulonephritis.

2011-03-17 | E-MEXP-2624 | biostudies-arrayexpress

Transcription profiling of human peripheral blood monocytes treated with Annexin A1 Ac1-25 vs. unstimulated

Project description:We used microarrays to detail the global gene expression changes elicited by stimulation of human peripheral blood monocytes from buffy coats with 50ÂµM Annexin A1 peptide Ac1-25 for 2h versus unstimulated control monocytes. Experiment Overall Design: three independent monocyte isolations each were used for stimulated and control cell RNA preparations and subsequent hybridization to arrays according to manufacturers protocols

2008-06-16 | E-GEOD-9080 | 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

Single-cell TCR-sequencing of T cells in crescentic glomerulonephritis

Project description:Single-cell TCR-sequencing of T cells in crescentic glomerulonephritis

| PRJNA924838 | ENA