Annexin A1 exerts renoprotective effects in experimental crescentic glomerulonephritis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA842654 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
Project description:We used microarrays to detail the global gene expression changes elicited by stimulation of human peripheral blood monocytes from buffy coats with 50µM Annexin A1 peptide Ac1-25 for 2h versus unstimulated control monocytes. Keywords: comparative gene expression study
2007-09-19 | GSE9080 | GEO
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
Project description:We used microarrays to detail the global gene expression changes elicited by stimulation of human peripheral blood monocytes from buffy coats with 50µM 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
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
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
Project description:Experimental autoimmune encephalomyelitis (EAE) is a mouse model for multiple sclerosis (MS) a chronic autoimmune disease of the central nervous system. We have observed dysfunction of the RNA binding protein hnRNP A1 in neurons from the brains of patients with MS, and the spinal cords of mice with EAE. Here, we sought to characterize the consequences of EAE-induced dysfunction of hnRNP A1 on the RNAs it binds by using CLIPseq to establish both the normal central nervous system RNA binding profile of hnRNP A1 in the spinal cords of naive mice, and any alterations to the binding profile of hnRNP A1 in the spinal cords of mice with EAE.
2024-01-04 | GSE208093 | GEO
Project description:In the present study, we used a functional proteomic approach to identify Annexin A1 (Anxa1) interacting proteins in the Philadelphia-positive KCL22 cell line. We focused on Anxa1 because it is one of the major proteins upregulated in imatinib-sensitive KCL22S cells versus imatinib-resistant KCL22R. Our proteomic strategy revealed 21 interactors. Bioinformatic analysis showed that most of these proteins are involved in cell death processes. Among the proteins identified, we studied the interaction of Anxa1 with two phosphatases, Shp1 and Shp2, which were recently identified as biomarkers of imatinib sensitivity in patients affected by chronic myeloid leukemia. Our data open new perspectives in the search for annexin-mediated signaling pathways and may shed light on mechanisms of resistance to imatinib that are unrelated to Bcr-Abl activity. For data analysis, we used the MASCOT software (version 2.4) Peptide Mass Fingerprinting search program (http://www.matrixscience.com) selecting NCBInr aug2010 database (11592891 sequences) (http://www.ncbi. nlm.nih.gov), and the following six parameters: specificity of the proteolytic enzyme used for hydrolysis (trypsin); up to 1 missed cleavage; cysteines such as S-carbamidomethylcysteines; unmodified N- and C-terminal ends; unmodified and oxidized methionines; putative Gln-induced pyroGlu formation; a precursor peptide maximum mass tolerance of 400 ppm, and a maximum fragment mass tolerance of 0.6 Da. Using the probability-based Mowse score, the ion score is 10 x Log(p), p being the probability that an eventual match is a random occurrence. All MS/MS spectra with a MASCOT score of or higher than 41 (p =< 0.05) had a good S/N, so the interpretation of the data was unambiguous. MS/MS spectra of peptides that had a MASCOT score below 41 were inspected manually and included in the statistics only in the presence of at least four continuous y or b ions.
2013-08-13 | PXD000030 | Pride
Project description:Innate lymphoid cells (ILCs) that express NK cell receptors (NCRs) and the transcription factor T-bet populate non-lymphoid tissues and are crucial in immune responses against viral infections and malignancies. Recent studies highlighted the heterogeneity of this ILC population and extended their functional spectrum to include important roles in tissue homeostasis and autoimmunity. Here, we provide detailed profiling of NCR+T-bet+ ILC populations in the murine kidney, identifying conventional NK (cNK) cells and type 1 ILCs (ILC1s) as the two major subsets. Induction of renal inflammation in a mouse model of glomerulonephritis did not substantially influence abundance or phenotype of cNK cells or ILC1s in the kidney. For functional analyses in this model, widely used depletion strategies for total NCR+ ILCs (αNK1.1 antibody application) and cNK cells (α-asGM1 serum application) were unreliable tools, since they were accompanied by significant off-target depletion of kidney NKT cells and CD8+ T cells, respectively. However, neither depletion of cNK cells and ILC1s in NKT cell-deficient mice, nor specific genetic deletion of cNK cells in Ncr1Cre/wt x Eomesfl/fl mice altered the clinical course of experimental glomerulonephritis. In summary, we show here that cNK cells and ILC1s are dispensable for initiation and progression of immune-mediated glomerular disease and advise caution in the use of standard antibody depletion methods to study NCR+ ILC function in mouse models.
2022-01-07 | GSE193001 | GEO
Project description:Conventional NK cells and ILC1s do not influence pathogenesis of experimental glomerulonephritis
| PRJNA794113 | ENA