Gene expression profile at single cell level from migrasomes injected and uninjected skin
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE269590 | GEO | 2025/06/17
REPOSITORIES: GEO
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Project description:In the present study, we have documented a previously unrecognized membrane vesicles called “migrasomes” (M-mig) that originate from the filament-like nanotubes of macrophage.To characterize the signatures of macrophage migrasomes (M-mig) gene expression that might underlie M-mig-associated biological function. M0-mig, M1-mig, M2-mig and HG-mig genome-wide expression profiling was carried out by using SurePrint G3 Mouse GE V2.0 8X60K Microarrays (Design ID:074809, Agilent Technologies, USA). Total RNA was quantified by the NanoDrop ND-2000 (Thermo Scientific) and the RNA integrity was assessed using Agilent Bioanalyzer 2100 (Agilent Technologies). The sample labeling, microarray hybridization and washing were performed based on the manufacturer’s standard protocols. Briefly, total RNA was transcribed to double strand cDNA, then synthesized into cRNA and labeled with Cyanine-3-CTP. The labeled cRNAs were hybridized onto the microarray. After washing, the arrays were scanned by the Agilent Scanner G2505C (Agilent Technologies). For data analysis, Feature Extraction software (version10.7.1.1, Agilent Technologies) was used to analyze array images to get raw data. Genespring (version14.9, Agilent Technologies) were employed to finish the basic analysis with the raw data. To begin with, the raw data was normalized with the quantile algorithm. Differentially expressed genes were then identified through fold change. The threshold set for up- and down-regulated genes was a fold change>=2.0. Afterwards, GO analysis and KEGG analysis were applied to determine the roles of these differentially expressed mRNAs.
2022-05-06 | E-MTAB-7994 | biostudies-arrayexpress
Project description:Gene expression profile at single cell level from migrasomes injected and uninjected skin
| PRJNA1122585 | ENA
Project description:Migrasomes, vesicular organelles generated on the retraction fibers of migrating cells, play a crucial role in migracytosis, mediating intercellular communication. The content cargoes determine the functional specificity of migrasomes. Migrasomes harbor numerous intraluminal vesicles, a pivotal component of their cargo. The mechanism underlying the transportation of these intraluminal vesicles to the migrasomes remain enigmatic. In this study, we identified a pathway by which Rab10-Caveolin1 mediates the transport of intraluminal vesicles to migrasomes. This intricate process necessitates the coordination of the motor protein Myosin Va, adaptor proteins RILPL2, facilitating vesicle transportation through retraction fibers to the migrasomes. Notably, the phosphorylation of Rab10 by the kinase LRRK2 augments this transport. Moreover, CSF-1 is selectively transported to migrasomes through this mechanism, subsequently fostering monocyte-macrophage differentiation in skin wound healing, which adds to our understanding of the physiological role of migrasomes.
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Project description:Conventional anti-angiogenic drugs (AADs) combined with sorafenib have little success in HCC patients, as the formation of hypoxia areas in tumors and vasculogenic mimicry’s (VM's) non-responsiveness to AADs. Migrasomes are recently discovered extracellular vesicles produced during cell migration. In this study, the results show that hypoxia-induced migrasomes induce the formation of VM and promote the sorafenib resistance. Further studies reveal that hypoxia-induced migrasomes can be taken up by HCC cells via macropinocytosis, which activates PI3K/AKT/TWIST1 signaling. Moreover, CD147 on the surface of hypoxia-induced migrasomes is identified as a key protein in regulating the signaling pathway. Overall, our findings uncover a previously unrecognized mechanism mediated by hypoxia-induced migrasomes and the formation of VM and provide a new method for preventing SFR.
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Project description:This dataset comprises bulk RNA-seq and scRNA-seq data derived from thymic tissues of stroke-induced murine models. The data investigate the therapeutic effects of bone marrow-derived mesenchymal stem cell (BM-MSC)-originated migrasomes on stroke-induced thymic atrophy and immunosuppression. The results highlight the mechanistic role of BM-MSC migrasomes in reversing thymic involution and the immunosuppressive state through the specific delivery of the Peptidylprolyl Cis/Trans Isomerase (Pin1) to thymic epithelial cells (TECs). This dataset serves as a valuable resource for understanding post-stroke immunosuppression and the molecular basis of BM-MSC/migrasome-mediated therapy.
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