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Project description:Tumor macrophages treated with exosomes
| PRJNA841486 | ENA
Project description:We performed a comprehensive miRNA profiling analysis of exosomes by Treponema pallidum-stimulated microarrays. A total of 2×106 macrophages were obtained by THP-1 differentiation and grown in RPMI-1640 containing 10% exosome-free FBS. Exosomes were acquired from macrophage culture supernatants with (n = 7) or without (n = 3) T. pallidum. Briefly, macrophages were washed in PBS twice and further grown in fresh medium for 12 h (n = 2), 24 h (n = 2) and 48 h (n = 3) to collect exosomes. Exosomal miRNA microarray assays were carried out with Agilent Human miRNA (8*60K) array.
2019-09-19 | GSE137637 | GEO
Project description:M2-polarized tumor-associated macrophages (TAMs) are a key factor contributing to the poor prognosis of pancreatic ductal adenocarcinoma (PDAC). While various factors within the tumor microenvironment drive their formation, the role of PDAC-derived exosomes in this process remains unclear. We aim to clarify the regulatory impacts of tumor-derived exosomes to TAMs. Through multi-Omics analysis, we identified CCT6A as a novel tumor-derived exosomal protein, bridging TAMs M2 polarization and PDAC prognosis. Co-culture with exosomes derived from CCT6Ahigh PDAC leads to greater M2 phenotype of TAMs via PI3K-AKT signaling. According to proteomics data, chemokines’ abundance reduces over tenfold once exosomal CCT6A absence, including CXCL1, CXCL3, CXCL20 and CCL5, whose interaction with CCT6A in PDAC cells was confirmed by interactomics data. Morever, we found CCT6A clearance abrogated the antagonism effects of CD47 antibody immunotherapy. The subunit of the T-complex protein Ring Complex (TRiC) CCT6A serves as a matchmaker, during exosomes-mediated chemokines transfer from PDAC to TAMs.
2025-05-26 | PXD056403 | Pride
Project description:This study aimed to elucidate the mechanism by which exosomes from bone-metastatic Lewis lung carcinoma (BM-LLC) cells promote osteolytic metastasis. We performed RNA-seq on mouse RAW264.7 macrophages (osteoclast precursors) treated with exosomes derived from either non-metastatic (NC-LLC) or bone-metastatic (BM-LLC) Lewis lung carcinoma cells. The goal was to identify differentially expressed genes and key regulatory pathways involved in exosome-induced osteoclast differentiation. Integrated analysis with small RNA sequencing data from the exosomes identified the miR-484-PECAM1 axis as a critical driver of this process. Our findings reveal that BM-LLC exosomes deliver miR-484 to recipient macrophages, repress PECAM1 expression, and subsequently upregulate osteoclastogenic markers (TRAP, CTSK, RANKL) and master transcription factors (NFATc1, c-Fos), thereby reprogramming osteoclastogenesis and driving bone destruction.
2025-12-31 | E-MTAB-15762 | biostudies-arrayexpress
Project description:Extracellular vesicles, such as exosomes, play a critical role in cell-to-cell communication and have been found to modulate cellular processes, including metabolic and inflammatory pathways, in recipient cells. Non-tuberculous Mycobacteria (NTM), such as Mycobacterium abscessus (M.ab), are a group of environmental bacteria that can cause severe lung infections in populations with pre-existing lung conditions, such as cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD). There is limited knowledge of the engagement of extracellular vesicles in the host-pathogen interactions in the context of NTM infections. In this study, we found that M.ab infection increased the release of a subpopulation of exosomes (CD9, CD63 and/or CD81 positive) by mouse macrophages but did not affect exosome morphology. Proteomic analysis of the vesicles demonstrated that M.ab infection affects the enrichment of host proteins in exosomes released by macrophages. When compared to exosomes from uninfected macrophages, exosomes released by M.ab-infected macrophages significantly improved M.ab growth and downregulated the intracellular level of glutamine in recipient macrophages in cell culture. Interestingly, the protein abundance of the glutamine transporters Slc1a5 and Slc38a2 were found to be enriched in exosomes from M.ab-infected macrophages compared to those from uninfected macrophages. Increasing glutamine concentration in the medium rescued intracellular glutamine levels and inhibited M.ab growth in recipient macrophages treated with exosomes from M.ab-infected macrophages. Taken together, our results indicate that exosomes may serve as extracellular glutamine eliminators that interfere with glutamine-dependent M.ab killing in recipient macrophages. This suggests that the development of exosome-targeting therapies may have the potential to augment current treatments for mycobacterial infections.
2025-05-07 | PXD052559 | Pride
Project description:Experiment Objective: To investigate the effects of recombinant complement protein on the expression levels of inflammatory cytokines and chemokines in macrophages. Experimental Design: Primary macrophages were isolated from the mouse peritoneal cavity. The macrophages were then treated with recombinant complement protein. Proteomics was performed to detect the differential expression of macrophage-related inflammatory cytokines and chemokines.
2026-06-16 | PXD079800 |
Project description:M2-polarized tumor-associated macrophages (TAMs) are a key factor contributing to the poor prognosis of pancreatic ductal adenocarcinoma (PDAC). While various factors within the tumor microenvironment drive their formation, the role of PDAC-derived exosomes in this process remains unclear. We aim to clarify the regulatory impacts of tumor-derived exosomes to TAMs. Through multi-Omics analysis, we identified CCT6A as a novel tumor-derived exosomal protein, bridging TAMs M2 polarization and PDAC prognosis. Co-culture with exosomes derived from CCT6Ahigh PDAC leads to greater M2 phenotype of TAMs via PI3K-AKT signaling. According to proteomics data, chemokines’ abundance reduces over tenfold once exosomal CCT6A absence, including CXCL1, CXCL3, CXCL20 and CCL5, whose interaction with CCT6A in PDAC cells was confirmed by interactomics data. Morever, we found CCT6A clearance abrogated the antagonism effects of CD47 antibody immunotherapy. The subunit of the T-complex protein Ring Complex (TRiC) CCT6A serves as a matchmaker, during exosomes-mediated chemokines transfer from PDAC to TAMs.
2025-04-06 | GSE278909 | GEO
Project description:M2-polarized tumor-associated macrophages (TAMs) are a key factor contributing to the poor prognosis of pancreatic ductal adenocarcinoma (PDAC). While various factors within the tumor microenvironment drive their formation, the role of PDAC-derived exosomes in this process remains unclear. We aim to clarify the regulatory impacts of tumor-derived exosomes to TAMs. Through multi-Omics analysis, we identified CCT6A as a novel tumor-derived exosomal protein, bridging TAMs M2 polarization and PDAC prognosis. Co-culture with exosomes derived from CCT6Ahigh PDAC leads to greater M2 phenotype of TAMs via PI3K-AKT signaling. According to proteomics data, chemokines’ abundance reduces over tenfold once exosomal CCT6A absence, including CXCL1, CXCL3, CXCL20 and CCL5, whose interaction with CCT6A in PDAC cells was confirmed by interactomics data. Morever, we found CCT6A clearance abrogated the antagonism effects of CD47 antibody immunotherapy. The subunit of the T-complex protein Ring Complex (TRiC) CCT6A serves as a matchmaker, during exosomes-mediated chemokines transfer from PDAC to TAMs.
2025-03-28 | GSE278339 | GEO
Project description:Mycobacterial transcripts were identified in exosomes released from M.tb infected RAW264.7 macrophages that were not present in uninfected exosomes suggesting export of mycobacterial RNA via exosomes Mycobacterial RNA was used as positive control and RNA from exosomes released from uninfected macrophages was used as negative control
2014-09-15 | GSE54444 | GEO
Project description:Macrophage-derived exosomes hold significant promise for clinical disease therapy. Macrophages can be categorized into several subtypes. The resting state is known as the M0 subtype, and the exosomes they secrete are termed M0-Exo. Macrophages can be polarized to the M2 subtype by combined induction with IL-4 and IL-13, and the exosomes derived from M2 macrophages are referred to as M2-Exo. miRNAs are important cargo within exosomes. Since both M0-Exo and M2-Exo exhibit therapeutic effects in inflammatory responses, we performed miRNA sequencing on the contents of M0-Exo and M2-Exo to investigate the underlying mechanisms of their therapeutic actions.
2026-01-23 | GSE312882 | GEO