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Effect of IL6 inhibition on the gene expression of erythroid progenitors in aged mice

ABSTRACT: Effect of IL6 inhibition on the gene expression of erythroid progenitors in aged mice

PROVIDER: PRJNA541910 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9029364.fastq.gz	Fastqsanger.gz
	SRR9029365.fastq.gz	Fastqsanger.gz
	SRR9029366.fastq.gz	Fastqsanger.gz
	SRR9029367.fastq.gz	Fastqsanger.gz
	SRR9029368.fastq.gz	Fastqsanger.gz

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Effect of IL6 inhibition on the gene expression of erythroid progenitors in aged mice

Project description:Gene expression analysis has revealed that Interleukin-6 signalling in murine erythroid progenitors is altered during ageing. Here we study the impact of inhibition of IL6 on the transcription profile of progenitors from bone marrow in aged mice

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Transcriptomic alterations of erythroid progenitors during ageing

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Mito-protective autophagy is impaired in erythroid cells of aged mtDNA-mutator mice

Project description:Somatic mitochondrial DNA (mtDNA) mutations contribute to the pathogenesis of age-related disorders, including myelodysplastic syndromes (MDS). The accumulation of mitochondria harboring mtDNA mutations in patients with these disorders suggests a failure of normal mitochondrial quality-control systems. The mtDNA-mutator mice acquire somatic mtDNA mutations via a targeted defect in the proofreading function of the mtDNA polymerase, PolgA, and develop macrocyticanemia similar to that of patients with MDS. We observed an unexpected defect in clearance of dysfunctional mitochondria at specific stages during erythroid maturation in hematopoietic cells from aged mtDNA-mutator mice. Mechanistically, aberrant activation of mechanistic target of rapamycin signaling and phosphorylation of uncoordinated 51-like kinase (ULK) 1 in mtDNA-mutator mice resulted in proteasome mediated degradation of ULK1 and inhibition of autophagy in erythroid cells. To directly evaluate the consequence of inhibiting autophagy on mitochondrial function in erythroid cells harboring mtDNA mutations in vivo, we deleted Atg7 from erythroid progenitors of wildtype and mtDNA-mutator mice. Genetic disruption of autophagy did not cause anemia in wild-type mice but accelerated the decline in mitochondrial respiration and development of macrocytic anemia in mtDNA-mutator mice. These findings highlight a pathological feedback loop that explains how dysfunctional mitochondria can escape autophagy-mediated degradation and propagate in cells predisposed to somatic mtDNA mutations, leading to disease. We used microarrays to identify expression profiles and pathways that are differentially activated or suppressed in Ter119+ bone marrow cells isolated from phlebotomized wildtype or Polg mutant mice

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Global gene expression prolife of primary cultured murine stress erythroid progenitors.

Project description:Inflammation inhibits steady state erythropoiesis, while at the same time it induces stress erythropoiesis to maintain erythroid homeostasis. Stress erythropoiesis relies on the rapid expansion of early progenitors that do not differentiate until the increase in serum Epo promotes a transition in progenitors to enable their synchronous differentiation. RNA-seq analysis allows us to identify an inflammatory transcriptome signature in early progenitors that induces iNOS-derived NO production. The accumulation of NO establishes a metabolism that promotes cell proliferation while inhibiting the differentiation of early progenitors. In contrast, the transition of progenitors to differentiation is marked by the suppressed inflammatory responses and a consequent decrease of iNOS-derived NO. We show that Epo initiates this transition response by altering progenitor metabolism to support itaconate production, resulting in the activation of Nrf2 that suppresses the inflammatory responses, which in turn alleviates the NO-mediated inhibition of erythroid program. Consequent differentiation of stress erythroid progenitors generates a bolus of new erythrocytes to maintain erythroid homeostasis until steady state erythropoiesis can resume.

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Impact of ERBB inhibitors on erythroid progenitors

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Transcriptomic alterations of erythroid progenitors during ageing

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Mito-protective autophagy is impaired in erythroid cells of aged mtDNA-mutator mice

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