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Targeting the tissue factor coagulation initiation complex prevents antiphospholipid antibody development.

ABSTRACT: Targeting the tissue factor coagulation initiation complex prevents antiphospholipid antibody development.

PROVIDER: PRJNA1060333 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27405834_1.fastq.gz	Fastqsanger.gz
	SRR27405834_2.fastq.gz	Fastqsanger.gz
	SRR27405835_1.fastq.gz	Fastqsanger.gz
	SRR27405835_2.fastq.gz	Fastqsanger.gz
	SRR27405836_1.fastq.gz	Fastqsanger.gz

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Targeting the tissue factor coagulation initiation complex prevents antiphospholipid antibody development.

Project description:Antiphospholipid antibodies (aPL) in primary or secondary antiphospholipid syndrome (APS) are a major cause for acquired thrombophilia. Here we show that specific inhibition of the TF coagulation initiation complex with nematode anticoagulant protein c2 (NAPc2) prevents the the development of persistent aPL and circulating phospholipid-reactive B1 cells in latent viral infection and lupus prone MRL-lpr mice. NGS mRNA profiling of splenic DC in lupus mice treated with NAPc2 versus saline control uncovered a suppression of dendritic cell activation in the spleen.

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Targeting the tissue factor coagulation initiation complex prevents antiphospholipid antibody development

Project description:Targeting the tissue factor coagulation initiation complex prevents antiphospholipid antibody development

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Project description:Antiphospholipid antibodies (aPL) in primary or secondary antiphospholipid syndrome (APS) areis a major cause for acquired thrombophilia. Here we test the effect of specific inhibition of the TF coagulation initiation complex with nematode anticoagulant protein c2 (NAPc2) on the activation of monocytes by aPL. NGS data show that aPL-induced proinflammatory and prothrombotic activation of monocytes, but not interferon regulated gene induction is prevent by NAPc2.

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Genetics of Antiphospholipid Antibody Syndrome (APS) - RTDC 5806

Project description:Genetics of Antiphospholipid Antibody Syndrome (APS) - RTDC 5806

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Transcriptomic Analysis of Placenta Affected by Antiphospholipid Antibodies: Following the TRAIL of trophoblast death

Project description:Antiphospholipid antibodies, a maternal risk factor for preeclampsia, increase shedding of necrotic trophoblast debris from the placenta, leading to endothelial dysfunction. Using Affymetrix HGU133 Plus 2 microarrays, we found changes in the transcriptome of placental explants treated with antiphospholipid antibodies including seven mRNAs encoding for genes BCL2L1, MCL1, PDCD2L, FASLG, SEMA6A, PRKCE and TRAIL that are involved in the regulation of apoptosis. Quantitative real-time RT-PCR and immunohistochemistry confirmed a reduction in TRAIL expression. These results may help to understand how antiphospholipid antibodies affect trophoblast cell death and how the antibodies could contribute to the pathogenesis of preeclampsia. Three different first-trimester placentas (8-8.5 weeks gestation) were dissected into 6 explants each and cultured either with antiphospholipid antibodies (25ug/mL) or untreated media for 16h. RNA was extracted from treated placental explants and Affymetrix HGU133 Plus 2 arrays were conducted to investigate changes in mRNA expression. Untreated: 1UNT, 2UNT, 3UNT Antiphospholipid antibody treatment: 1APL, 2APL, 3APL Biological replicates: 1, 2, 3

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