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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.

2025-03-01 | GSE282740 | GEO

Csf1<sup>+</sup> AD-MSCs promote stroke repair by activating the resident microglia.

Project description: Not available

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G-CSF1

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RNAseq of untreated and CSF1-treated, CSF1+QVD-treated monocytes

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). 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. This study confirms the importance of caspase activation in CSF1 differentiation.

2024-01-01 | E-MTAB-8088 | biostudies-arrayexpress

Differential Roles of Astrocytic CSF1 in Alzheimer's Disease and Cerebral Amyloid Angiopathy: Insights from Transcriptomic Analysis

Project description:Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA) are neurodegenerative disorders characterized by the pathological deposition of amyloid-beta (Aβ) in the brain. Although both conditions share common pathogenic pathways, they exhibit distinct cellular manifestations and disease progression. Our study focused on the differential expression and role of astrocytic colony-stimulating factor 1 (CSF1) in these diseases. Using transcriptomic analysis of 248 brain tissue samples from the hippocampal-entorhinal system of 50 individuals, we identified a significant increase in CSF1 expression in the CA4 subfield of AD patients compared to a marked decrease in CAA. Functional investigations revealed that astrocytes with elevated CSF1 levels displayed neurotoxicity associated with AD-like pathology, whereas reduced CSF1 expression in astrocytes was linked to vascular damage typical of CAA. These findings suggest that CSF1 plays divergent roles in AD and CAA, contributing to their distinct pathological profiles. Our study highlights the potential of targeting astrocytic CSF1 expression as a differential diagnostic marker and therapeutic approach in managing these overlapping yet distinct neurological conditions.

2024-12-15 | GSE278723 | GEO

RNAseq of untreated, CSF1-treated, CSF1+QVD-treated, and GM-CSF-treated monocytes

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.

2024-01-01 | E-MTAB-5752 | biostudies-arrayexpress

Expression data from CD73 positive adipose derived mesenchymal stem cells (CD73+ AD-MSCs) and CD73 negative adipose derived mesenchymal stem cells (CD73- AD-MSCs) of mouse

Project description:MSCs are a heterogeneous population and the specific population of MSCs may exhibit a selective ability for tissue repair. The aim of our research was to adapt the CD73+ subgroup of adipose derived MSCs (AD-MSCs) for the therapy of myocardial infarction (MI). Our results revealed that CD73+ AD-MSCs played more effective role in the acceleration function of cardiac recovery by promoting angiogenesis in a rat model of MI compared to mixed AD-MSCs and CD73- AD-MSCs. Microarray analysis shows differences between CD73+ and CD73- AD-MSCs when transcription profile of these two subgroups were compared, especially in VEGF pathway.

2021-06-02 | GSE167219 | GEO

RNAseq of untreated and CSF1-treated, CSF1+QVD-treated monocytes

Project description:RNAseq of untreated and CSF1-treated, CSF1+QVD-treated monocytes

| PRJEB33182 | ENA

Robust Neurogenesis in Chronic Stroke Monkeys Following Mesenchymal Stem Cell Transplantation Plus Intermittent Theta-burst Stimulation

Project description:A significant population of chronic stroke patients urgently requires more effective therapies due to functional plateaus and limited intervention options. Intermittent theta-burst stimulation (iTBS) has been increasingly adopted in chronic-phase ischemic stroke management. However, the efficacy decreases over time. Mesenchymal stem cells (MSCs) have emerged as a promising therapeutic strategy for chronic stroke management through multiple mechanisms. Whether combined MSC transplantation and iTBS confers superior synergistic efficacy warrants further investigation. In this study, human umbilical cord-derived MSCs were stereotactically injected into the penumbra of the brain parenchyma adjacent to infarct sites in cynomolgus monkeys with chronic-stage middle cerebral artery occlusion (MCAO)-induced ischemic stroke. iTBS commenced at 1 week post-transplantation (5 sessions/week until week 17). Behavioral tests, electrophysiological recordings, functional magnetic resonance imaging (fMRI), magnetic resonance spectroscopy (MRS), and plasma proteomic analysis were conducted longitudinally, with terminal histological and spatial proteomic analysis at week 17. The results demonstrated that combined MSC/iTBS therapy enhanced motor function, reduced cortical excitation thresholds, shortened motor-evoked potential (MEP) latency, increased neural activity intensity/synchronization, strengthened functional connectivity, and optimized motor cortex metabolism. In addition to the commonly attributed therapeutic mechanisms of MSCs and iTBS, the combined therapy additionally triggered neurogenesis and stem cell chemotaxis, which was potentially mediated by iTBS-enhanced CXCL12 secretion from MSCs. Therefore, MSC/iTBS combination therapy can effectively treat chronic stroke through multiple mechanisms, particularly involving the activation of endogenous neural stem cells (NSCs), representing a promising interdisciplinary treatment strategy.

2026-03-12 | PXD071582 | Pride

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