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Isolevuglandins disrupt PU.1 mediated C1q expression and promote autoimmunity and hypertension in systemic lupus erythematosus

ABSTRACT: Isolevuglandins disrupt PU.1 mediated C1q expression and promote autoimmunity and hypertension in systemic lupus erythematosus

PROVIDER: PRJNA824809 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18685877_1.fastq.gz	Fastqsanger.gz
	SRR18685877_2.fastq.gz	Fastqsanger.gz
	SRR18685878_1.fastq.gz	Fastqsanger.gz
	SRR18685878_2.fastq.gz	Fastqsanger.gz
	SRR18685879_1.fastq.gz	Fastqsanger.gz

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Isolevuglandins disrupt PU.1-mediated C1q expression and promote autoimmunity and hypertension in systemic lupus erythematosus.

Project description:We describe a mechanism responsible for systemic lupus erythematosus (SLE). In humans with SLE and in 2 SLE murine models, there was marked enrichment of isolevuglandin-adducted proteins (isoLG adducts) in monocytes and dendritic cells. We found that antibodies formed against isoLG adducts in both SLE-prone mice and humans with SLE. In addition, isoLG ligation of the transcription factor PU.1 at a critical DNA binding site markedly reduced transcription of all C1q subunits. Treatment of SLE-prone mice with the specific isoLG scavenger 2-hydroxybenzylamine (2-HOBA) ameliorated parameters of autoimmunity, including plasma cell expansion, circulating IgG levels, and anti-dsDNA antibody titers. 2-HOBA also lowered blood pressure, attenuated renal injury, and reduced inflammatory gene expression uniquely in C1q-expressing dendritic cells. Thus, isoLG adducts play an essential role in the genesis and maintenance of systemic autoimmunity and hypertension in SLE.

| S-EPMC9310530 | biostudies-literature

Isolevuglandins disrupt PU.1 mediated C1q expression and promote autoimmunity and hypertension in systemic lupus erythematosus

Project description:To determine the gene expression of profile of dendritic cells (DCs) from lupus prone mice we sorted CD11c+ cells from 4 7 week old female C57Bl/6 mice and 4 7 week old B6.SLE123 mice. We then performed gene expression profiling analysis using data obtained from RNA-seq from DCs of these 8 animals.

2022-04-13 | GSE200485 | GEO

Circadian Clock Protein CRY Regulates Autoimmunity

Project description:The circadian system regulates numerous physiological processes including the adaptive immune system. Here we show that mice deficient for the circadian genes Cry1 and Cry2, (DKO) display an autoimmune phenotype including higher serum IgG concentration, presence of serum anti-nuclear antibodies, precipitation of IgG, IgM and complement 3 in glomeruli, and massive infiltrations of leukocytes into the lung and kidney. Activation of Cry DKO splenic B cells elicited markedly enhanced and prolonged tyrosine phosphorylation of cellular proteins compared to cells from control mice, suggesting that over activation of the BCR signaling pathway may contribute to autoimmunity in the Cry DKO mice. Expression of C1q, deficiency of which contributes to the pathogenesis of Systemic lupus erythematosus (SLE), was significantly downregulated in Cry DKO B cells. This suggests that B cell development, BCR signaling pathway and C1q expression may be under direct circadian control and dysregulation of which contributes to autoimmunity.

2018-08-24 | GSE87467 | GEO

C1q elicited macrophage gene expression

Project description:We have data from a previous microarray experiment which shows that C1q elicits macrophages to express genes important for clearance of dead (apoptotic) cells. In this experiment we want to determine the signaling mechanism by which C1q is turning on macrophage gene expression. For our control (sample 1-3) we heated C1q to denature it so it is inactive. We also want to know which portion of C1q is responsible for activation the macrophage so we generated C1qtails (samples 4-5). We also have macrophages treated with the whole C1q molecule (7-9). And finally we have a cell line (J774) treated with C1q but does not activate the cells (samples 10-12). Bone marrow derived macrophages or J774 cells were adhered to heat inactivated C1q, C1q tails or C1q for 18 hours. Cells were harvested and RNA was isolated and converted to double stranded cDNA and subsequently labeled and hybridized onto NimbleGen mouse gene expression array [100718_MM9_EXP] using Nimblegen Hybridization system 4 according to manufacturerM-bM-^@M-^Ys instructions (Roche)

2014-07-10 | E-GEOD-48619 | biostudies-arrayexpress

C1q elicited macrophage gene expression

2014-07-10 | GSE48619 | GEO

Gene expression analysis in complex canine chronic cutaneous lupus erythematosus (CCLE)

Project description:We performed a comparative immunology case study of client-owned dogs to determine if immune and skin gene expression profiles in spontaneous canine chronic cutaneous lupus erythematosus (CCLE) with concomitant systemic autoimmunity mirror those observed in human CCLE.

2022-02-11 | GSE180276 | GEO

PU.1

Project description:PU.1

| PRJNA344317 | ENA

Transcriptome analysis of C1q-administrated murine lungs

Project description:Pulmonary fibrosis (PF) is a progressive fibrotic disease with a poor prognosis and suboptimal therapeutic options. The complement molecule C1q, which plays an important role in the phagocytic capacity of macrophages, has recently been reported to exacerbate several fibrosis-related diseases. On the other hand, there are still no reports in PF. Here, we analyzed gene expression changes of C1q-administrated murine lungs.

2024-03-31 | GSE184445 | GEO

Transcriptome analysis of C1q treated lung fibroblasts

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Regulation of neuronal gene and miRNA expression by the complement protein C1q associated with neuroprotection

Project description:Identification of transcriptional profiles stimulated by the complement protein C1q in rat immature neurons associated with the C1q-dependent neuroprotection observed in vitro. Use of the unbiased whole genome microarray approach to identify genes regulated by C1q. Immature neurons grown in vitro for 3 days were stimulated with 10 nM C1q for 3h.

2011-03-07 | E-GEOD-18860 | biostudies-arrayexpress

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