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Altered microRNA expression links IL6 and TNF-induced inflammaging with myeloid malignancy [miR146aKO_ESLAM_SCBS]

ABSTRACT: Altered microRNA expression links IL6 and TNF-induced inflammaging with myeloid malignancy [miR146aKO_ESLAM_SCBS]

PROVIDER: PRJNA626673 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11576300_1.fastq.gz	Fastqsanger.gz
	SRR11576300_2.fastq.gz	Fastqsanger.gz
	SRR11576301_1.fastq.gz	Fastqsanger.gz
	SRR11576301_2.fastq.gz	Fastqsanger.gz
	SRR11576302_1.fastq.gz	Fastqsanger.gz

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Altered microRNA expression links IL6 and TNF-induced inflammaging with myeloid malignancy

Project description:Altered microRNA expression links IL6 and TNF-induced inflammaging with myeloid malignancy

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Altered microRNA expression links IL6 and TNF-induced inflammaging with myeloid malignancy [miR146aKO_LSK_WGBS]

Project description:Aging is associated with significant changes in the hematopoietic system, including increased inflammation, impaired hematopoietic stem cell (HSC) function, and increased incidence of myeloid malignancy. Inflammation of aging (“inflammaging”) has been proposed as a driver of age-related changes in HSC function and myeloid malignancy, but mechanisms linking these phenomena remain poorly defined. Here, we identify loss of miR-146a as driving aging-associated inflammation in AML patients. miR-146a expression declined in old wild-type mice, and loss of miR-146a promoted premature HSC aging and inflammation in young miR-146a-null mice, preceding development of aging-associated myeloid malignancy. Using single-cell assays of HSC quiescence, stemness, differentiation potential, and epigenetic state to probe HSC function and population structure, we found that loss of miR-146a depleted a subpopulation of primitive, quiescent HSCs. DNA methylation and transcriptome profiling implicated NF-κB, IL6, and TNF as potential drivers of HSC dysfunction, activating an inflammatory signaling relay promoting IL6 and TNF secretion from mature miR-146a-/- myeloid and lymphoid cells. Reducing inflammation by targeting Il6 or Tnf was sufficient to restore single-cell measures of miR-146a-/- HSC function and subpopulation structure, and reduced the incidence of hematological malignancy in miR 146a-/- mice. miR-146a-/- HSCs exhibited enhanced sensitivity to IL6 stimulation, indicating that loss of miR-146a affects HSC function via both cell-extrinsic inflammatory signals and increased cell-intrinsic sensitivity to inflammation. Thus, loss of miR 146a regulates cell-extrinsic and -intrinsic mechanisms linking HSC inflammaging to the development of myeloid malignancy.

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Altered microRNA expression links IL6 and TNF-induced inflammaging with myeloid malignancy [miR146aKO_ESLAM_SCBS]

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Altered microRNA expression links IL6 and TNF-induced inflammaging with myeloid malignancy [miR146aKO_LSK_WGBS]

Project description:Altered microRNA expression links IL6 and TNF-induced inflammaging with myeloid malignancy [miR146aKO_LSK_WGBS]

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Altered microRNA expression links IL6 and TNF-induced inflammaging with myeloid malignancy

Project description:This SuperSeries is composed of the SubSeries listed below.

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Effect of anti-TNF/IL-6 NANOBODY® VHH, Humira, Sylvant, TNF, IL6 and TNF+IL6 in RA-FLS/T cell cocultures

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Project description:Aging is characterized by a chronic low-grade inflammation in multiple tissues, also termed as “inflammaging”, which represents a significant risk factor for many aging-related chronic diseases. However, the mechanisms and regulatory networks behind inflammaging across different tissues have not been fully elucidated. Here, by profiling transcriptomes and epigenomes of the kidney and liver from young and aged mice, we found that activation of inflammatory response was the conserved signature across tissues. Through integrative analysis, we revealed links between transcriptome change and chromatin dynamics, and identified AP-1 and ETS family transcription factors (TFs) were potential regulators of inflammaging. Further in-situ validation showed AP-1 was mainly activated in aged hepatic and renal cells, while enhanced ETS was almost caused by elevated infiltration of macrophages, indicating these TFs had different mechanisms in inflammaging. Functional data showed genetic knockdown of Fos, a major member of AP-1, significantly attenuated inflammatory response in aged kidneys and livers. Taken together, our analysis revealed conserved signatures and regulatory TFs of inflammaging in the kidney and liver, providing novel targets for the development of anti-aging interventions.

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2021-03-22 | PXD024356 | Pride

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