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Csf1+ AD-MSCs promote stroke repair by activating the resident microglia

ABSTRACT: Csf1+ AD-MSCs promote stroke repair by activating the resident microglia

PROVIDER: PRJNA1190126 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31482777_1.fastq.gz	Fastqsanger.gz
	SRR31482777_2.fastq.gz	Fastqsanger.gz
	SRR31482778_1.fastq.gz	Fastqsanger.gz
	SRR31482778_2.fastq.gz	Fastqsanger.gz
	SRR31482779_1.fastq.gz	Fastqsanger.gz

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Csf1+ AD-MSCs promote stroke repair by activating the resident microglia

Project description:We have employed a single cell sequencing approach using 10x Genomics scRNAseg to study the mechanism of AD-MSCs for treating the injured brain tissue. This study establishes a rat model of hemorrhagic stroke, followed by intravenous infusion of allogeneic AD-MSCs 24 hours post-model induction, in order to observe the therapeutic effect and analyze the underlying mechanism of action. Based on single-cell transcriptomic sequencing technology, we demonstrated that the re-infusion of AD-MSCs 24 hours after stroke mainly promotes the repair of injured brain tissue by activating brain tissue resident microglia and inhibiting bone marine-derived monocytes. Importantly, this role depends on the cell subsets of AD-MSCs that are highly expressing Csf1+. This study offers novel insights into the mechanisms underlying MSC-based stroke treatment and supports the potential for stable and efficacious MSC therapies.

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Project description:Caspases, which are key effectors of apoptosis, have demonstrated non-apoptotic functions. One of these functions is the differentiation into macrophages of peripheral blood monocytes exposed to Colony-Stimulating Factor-1 (CSF1). Conversely, GM-CSF induces the differentiation of monocytes into macrophages in a caspase-independent manner. Macrophages generated by CSF1 and GM-CSF have distinct polarity. Macrophage polarization plays an important role in the pathogenesis of diverse human diseases as cancer, leading us to explore if caspase inhibition would affect macrophage polarization. To explore the role of caspases in CSF1 differentiation, we used human monocytes sorted from buffy coats treated by cytokines. We reported that caspase inhibition delays the ex vivo differentiation of peripheral blood monocytes exposed to CSF1 and modifies the phenotype of generated macrophages, e.g. cell shape, surface markers. Moreover, by RNAseq, we observed that the macrophages generated in presence of CSF1 and QVD are different from CSF1-treated monocytes and from GM-CSF-treated monocytes. Cell cycle and focal adhesion-related pathway genes were selectively down-regulated. This study confirms the importance of caspase activation in CSF1 differentiation.

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