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Innate immune memory after brain injury drives inflammatory cardiac dysfunction [CUT&tag]

ABSTRACT: Innate immune memory after brain injury drives inflammatory cardiac dysfunction [CUT&tag]

PROVIDER: PRJNA1102377 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28746766_1.fastq.gz	Fastqsanger.gz
	SRR28746766_2.fastq.gz	Fastqsanger.gz
	SRR28746767_1.fastq.gz	Fastqsanger.gz
	SRR28746767_2.fastq.gz	Fastqsanger.gz
	SRR28746768_1.fastq.gz	Fastqsanger.gz

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Innate immune memory after brain injury drives inflammatory cardiac dysfunction [CUT&tag]

Project description:The enormous medical burden of stroke is not only due to the brain injury itself and the acute systemic effects, but is largely determined by chronic comorbidities that develop secondarily after stroke. We hypothesized that the high rate of comorbidity developing after a stroke might have a shared immunological cause, however, the chronic effects of brain injury on systemic immunity have so far been barely investigated. Here, we identified myeloid innate immune memory as a cause of remote organ dysfunction after stroke. Using single-cell sequencing, we identified persistent pro-inflammatory transcriptomic changes in resident monocytes/macrophages in multiple organs one month after experimental ischemic brain injury, which was particularly abundant in the heart and associated with the development of cardiac fibrosis and diastolic dysfunction. A similar phenotype was seen in myocardial autopsy samples from stroke versus control patients. We observed chronic functional changes in myeloid hematopoiesis driven by post-stroke IL-1-mediated epigenetic changes. These alterations could be transplanted to naïve recipient mice and were sufficient to induce cardiac dysfunction. By effectively blocking the trafficking of pro-inflammatory monocytes from the bone marrow to the heart using a dual CCR2/5 inhibitor, we successfully prevented post-stroke cardiac dysfunction. This approach holds promising potential as a novel immune-targeted secondary prevention therapy. We anticipate that the epigenetic immune reprogramming mechanisms detailed here for the brain-heart axis could be generalized to provide a novel framework for explaining the development of various comorbidities after acute tissue injury in remote organs.

2024-07-22 | GSE264418 | GEO

HCT116_SMARCA4 CUT&Tag

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CUT&TAG of OE19 cell line

Project description:To map the chromatin binding sites for SMC1 in OE19 cells, we performed CUT&TAG.

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CUT&TAG of OE19 cell line

Project description:To map the chromatin binding sites for various factors in OE19 cells, we performed CUT&TAG.

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Bulk Cut&run and Cut&tag

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scNanoSeq-CUT&Tag: a long-read single-cell CUT&Tag sequencing method for efficient chromatin modification profiling within individual cells

Project description:We developed scNanoSeq-CUT&Tag, a streamlined method by adapting a modified CUT&Tag protocol to Oxford Nanopore sequencing platform for efficient chromatin modification profiling at single-cell resolution. We firstly tested the performance of scNanoSeq-CUT&Tag on six human cell lines: K562, 293T, GM12878, HG002, H9, HFF1 and adult mouse blood cells, it showed that scNanoSeq-CUT&Tag can accurately distinguish different cell types in vitro and in vivo. Moreover, scNanoSeq-CUT&Tag enables to effectively map the allele-specific epigenomic modifications in the human genome andallows to analyze co-occupancy of histone modifications. Taking advantage of long-read sequencing,scNanoSeq-CUT&Tag can sensitively detect epigenomic state of repetitive elements. In addition, by applying scNanoSeq-CUT&Tag to testicular cells of adult mouse B6D2F1, we demonstrated that scNanoSeq-CUT&Tag maps dynamic epigenetic state changes during mouse spermatogenesis. Finally, we exploited the epigenetic changes of human leukemia cell line K562 during DNA demethylation, it showed that NanoSeq-CUT&Tag can capture H3K27ac signals changes along DNA demethylation. Overall, we prove that scNanoSeq-CUT&Tag is a valuable tool for efficiently probing chromatin state changes within individual cells.

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Innate immune memory after brain injury drives inflammatory cardiac dysfunction

Project description:Innate immune memory after brain injury drives inflammatory cardiac dysfunction

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Cut&Tag of GLI3 binding during early organoid development

Project description:To investigate GLI3 TF targets during organoid fate decisions, we performed Cut&Tag of GLI3 binding

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HCT116_SMARCA4 CUT&Tag

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2022-09-04 | GSE212334 | GEO

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Project description:We performed the cleavage under targets and tagmentation (Cut & tag) assay followed by sequencing enriched DNA fragments to reveal the direct downstream targets of Pbx1. Firstly, we overexpressed Pbx1b with Pbx1b-IRES-GFP retrovirus in murine peripheral B cells to ensure the yields of DNA fragments. CUT & tag libraries were generated following instructions of the manufacturer’s protocol (Vazyme; cat TD901-01) and the Pbx1 antibody (CST; cat 4342) was used for signal enrichment.

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