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Severe infection constitutively upregulates TIMP1 in the bone marrow hematopoietic niche to support long-term enhanced myelopoiesis

ABSTRACT: Severe infection constitutively upregulates TIMP1 in the bone marrow hematopoietic niche to support long-term enhanced myelopoiesis

PROVIDER: PRJNA847242 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19589068.fastq.gz	Fastqsanger.gz
	SRR19589069.fastq.gz	Fastqsanger.gz

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Severe infection constitutively upregulates TIMP1 in the bone marrow hematopoietic niche to support long-term enhanced myelopoiesis

Project description:Infection is able to elicit innate immunological memory by enhancing a long-term myeloid output even after the inciting infectious agent has been cleared. However, mechanisms underlying such a regulation are not fully understood. Using a mouse polymicrobial peritonitis (sepsis) model, we show that severe infection leads to increased, sustained myelopoiesis after the infection is resolved. The infection experience is imprinted in the bone marrow (BM) stromal cells, in the form of a constitutive upregulation of the tissue inhibitor of metalloproteinases 1 (TIMP1). TIMP1 antagonizes the function of ADAM10, an essential cleavage enzyme for the activation of Notch which in turn suppresses myelopoiesis. While TIMP1 is dispensable for myelopoiesis under the steady state, increased TIMP1 enhances myelopoiesis post infection. Thus, our data reveal that infection could establish an inflammatory memory in the BM niche to support a long-term enhanced output of innate immune cells.

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Global miRNA expression status of human hematopoietic stem–progenitor cells modulates myelopoiesis

Project description:We investigated how suppression of the most upstream microRNA–processing RNase, Drosha, affects the differentiation of human CD34+ hematopoietic stem–progenitor cells (HSPCs). We hypothesized that knock-down of Drosha would alter blood lineage development by modulating the expression of microRNAs. Lentiviral delivery to HSPCs of a short-hairpin targeting Drosha resulted in a viable phenotype with promotion of myeloid, and especially monocytic, maturation and suppression of apoptosis. Our results show that Drosha deficiency triggered a parallel upregulation of components of the RNAi machinery, including DGCR8, Dicer and Ago2. Deep sequencing analyses revealed global miRNA deficiency after Drosha short-hairpin treatment with relative maintenance of mature miR-223 expression. Restoration of miR-223 to normal levels after Drosha knock-down further enhanced monocytic maturation concomitant with the modulation of myeloid transcription factors that promoted monocytic differentiation. Our results support a miRNA accentuation model in which relative enhancement of miR-223 increases levels of PU.1 thereby promoting monocytic differentiation. CD34+ HSPCs were isolated from umbilical cord blood and transduced with an empty lentivector (EV) or a lentivector encoding a short-hairpin RNA targeting the pri-miRNA–processing enzyme, Drosha (shDrosha). EV and shDrosha transduced HSPCs were grown in liquid culture promoting myelopoiesis and sampled on days 0 and 7 for total RNA collection. Total RNA was size fractionated to enrich for the small RNA population and deep sequenced using ABI's SOLiD 4.0 platform.

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