LncRNA Gm26917 promotes macrophage differentiation by enhancing Annexin A1 ubiquitination in LPS-induced acute liver injury
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA770618 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16297072_1.fastq.gz | Fastqsanger.gz | |||
| SRR16297072_2.fastq.gz | Fastqsanger.gz | |||
| SRR16297073_1.fastq.gz | Fastqsanger.gz | |||
| SRR16297073_2.fastq.gz | Fastqsanger.gz | |||
| SRR16297074_1.fastq.gz | Fastqsanger.gz |
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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: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:Long noncoding RNAs (lncRNAs) are defined as transcripts of more than 200 nucleotides that have little or no coding potential. LncRNAs function as key regulators in diverse physiological and pathological processes. However, the roles of lncRNAs in lipopolysaccharide (LPS)-induced acute liver injury (ALI) are still elusive. In this study, we report the roles of lncRNA Gm26917 induced by LPS in modulating liver inflammation. As key components of the innate immune system, macrophages play critical roles in the initiation, progression and resolution of ALI. Our studies demonstrated that Gm26917 localized in the cytoplasm of hepatic macrophages and globally regulated the expression of inflammatory genes and the 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 the 3'-truncation of Gm26917 interacted with the N-terminus of Annexin A1, a negative regulator of the 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. In addition, expression of Gm26917 in inflammatory macrophages was regulated by the transcription factor forkhead box M1 (FOXM1). LPS treatment dramatically increased the binding of FOXM1 to the promoter region of Gm26917 in macrophages. In summary, our findings suggest that lncRNA Gm26917 silencing protects against LPS-induced liver injury by regulating the TLR4/NF-κB signaling pathway in macrophages.
| S-EPMC9663662 | biostudies-literature
Project description:Annexin A1 exerts renoprotective effects in experimental crescentic glomerulonephritis
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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
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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: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:We have generated immune-enhancing neutrophils by culturing murine primary bone marrow derived neutrophils with either super-low dose of LPS. Immune-enhancing neutrophils preferentially express co-stimulatory molecules such as CD74, CD44 and CD86, and exhibit reduced expression of CD11b. Purified bone marrow neutrophils were treated with PBS or 100 pg/ml LPS overnight in the presence of GM-CSF, and harvested for scRNAseq analysis to examine their profiles of gene expression.
2024-05-17 | GSE230237 | GEO
Project description:Oriented cell divisions are critical for the formation and maintenance of structured epithelia. Proper mitotic spindle orientation relies on polarised anchoring of force generators to the cell cortex by the evolutionarily conserved Gαi-LGN-NuMA complex. However, the polarity cues that control cortical patterning of this ternary complex remain largely unknown in mammalian epithelia. Here we identify the membrane-associated protein Annexin A1 (ANXA1) as a novel interactor of LGN in mammary epithelial cells. ANXA1 acts independently of Gαi to instruct the accumulation of LGN and NuMA at the lateral cortex to ensure cortical anchoring of Dynein-Dynactin and astral microtubules and thereby planar alignment of the mitotic spindle. Loss of ANXA1 randomises mitotic spindle orientation, which in turn disrupts epithelial architecture and lumen formation in three-dimensional (3D) primary mammary organoids. Our findings establish ANXA1 as an upstream cortical cue that regulates LGN to direct planar cell divisions during mammalian epithelial morphogenesis.
2022-12-02 | PXD027452 | Pride