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Granulocyte-monocyte progenitor (GMP) RNA-seq in wild type and MST1-deficient mice.

ABSTRACT: We sorted granulocyte-monocyte progenitor from wild-type and MST1-deficient mice by flow cytometry and performed transcriptome sequencing, analysis of differentially expressed genes, signaling pathways, metabolic pathways, etc. in the absence of MST1.

ORGANISM(S): Mus musculus

PROVIDER: GSE213143 | GEO | 2023/12/01

REPOSITORIES: GEO

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Granulocyte-monocyte progenitor (GMP) RNA-seq in wild type and MST1-deficient mice.

Project description:Granulocyte-monocyte progenitor (GMP) RNA-seq in wild type and MST1-deficient mice.

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Wild-type and tafazzin-deficient clones of granulocyte-monocyte progenitors (GMP), ER-HOXB8 conditionally immortalized, immature, in estrogen.

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Project description:Calcium pyrophosphate dihydrate (CPPD) crystals are formed locally within the joints, leading to pseudogout. Although the mobilization of local granulocytes can be observed in joints where pseudogout has manifested, the mechanism of this activity remains poorly understood. In this study, CPPD crystals were administered to mice, and the dynamics of splenic and peripheral blood myeloid cells were analyzed. As a result, levels of both granulocytes and monocytes were found to increase following CPPD crystal administration in a concentration-dependent manner, with a concomitant decrease in lymphocytes in the peripheral blood. In contrast, the levels of other cells, such as dendritic cell subsets, T-cells, and B-cells, remained unchanged in the spleen, following CPPD crystal administration. Furthermore, an increase in granulocytes/monocyte progenitors (GMPs) and a decrease in megakaryocyte/erythrocyte progenitors (MEPs) were also observed in the bone marrow. In addition, CPPD administration induced production of IL-1β, which acts on hematopoietic stem cells and hematopoietic progenitors and promotes myeloid cell differentiation and expansion. These results suggest that CPPD crystals act as a "danger signal" to induce IL-1β production, resulting in changes in course of hematopoietic progenitor cell differentiation and in increased granulocyte/monocyte levels, and contributing to the development of gout.

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