bims-migras Biomed News
on Migrasomes
Issue of 2025–11–16
five papers selected by
Cliff Dominy



  1. Mol Med Rep. 2026 Jan;pii: 36. [Epub ahead of print]33(1):
      Migrasomes are novel extracellular organelles that were first reported in 2015. The present review summarizes the discovery, structural characteristics, biological functions and relationships of this new cellular organelle with diseases. Migrasomes are annular organelles that extend from the trailing edge of cells during cell migration and are rich in proteins, lipids, nucleic acids and other biomolecules. They serve important roles at multiple levels, including roles in cell‑cell communication, tissue remodeling and immune regulation. The formation and function of migrasomes are associated with the regulation of various molecules and signaling pathways, including nucleation, expansion and maturation. Migrasomes also have important roles in organ morphogenesis, angiogenesis, mitochondrial quality control and immune regulation. In addition, migrasomes are closely associated with the development of various diseases, including kidney diseases, pneumonia after stroke, neurodegenerative diseases and cancer, providing new perspectives and potential targets for disease diagnosis and treatment. For example, in cancer, migrasomes can act as positioning signals, regulating the invasion of liver cancer cells. In neurodegenerative diseases, migrasomes may have a role in clearing damaged mitochondria, thereby helping to alleviate inflammatory responses and cellular dysfunction. Collectively, these findings suggest that migrasomes have notable potential for use in clinical disease diagnosis and treatment.
    Keywords:  biomarkers; cell migration; cell‑cell communication; migrasomes; mitochondrial quality control
    DOI:  https://doi.org/10.3892/mmr.2025.13746
  2. Cell Commun Signal. 2025 Nov 10. 23(1): 483
      Migrasomes are organelles that play important roles in cell communication, development, angiogenesis, and other cellular processes. It is crucial for investigators to collect migrasomes from both in vitro and in vivo sources. Traditionally, trypsin-EDTA has been used to harvest migrasomes from in vitro-cultured cells. However, our work demonstrated that treatment with trypsin-EDTA might cause the disappearance of migrasomes, thus reducing the efficiency of migrasome harvesting. By employing a low concentration of NP-40, we could fracture the retraction fibers between the migrasome and the cell body. Through the treatment of low-concentration NP-40 followed by trypsin-EDTA, we developed a new method for harvesting migrasomes, considerably increasing the harvesting efficiency. Our work provides new insights into the fundamental barriers that remain in the investigation of migrasomes.
    DOI:  https://doi.org/10.1186/s12964-025-02495-3
  3. Elife. 2025 Nov 13. pii: RP97621. [Epub ahead of print]13
      The growing ability of pathogens and tumor cells to evade immune surveillance underscores the urgent need for new vaccine platforms that harness diverse biological mechanisms. Logistical constraints associated with cold-chain transport further limit vaccine accessibility, particularly in resource-limited settings. Migrasomes-specialized organelles produced during cell migration-are inherently stable and enriched with immune-modulating molecules. To overcome the low yield of natural migrasomes, we engineered migrasome-like vesicles (eMigrasomes) using hypotonic shock combined with cytoskeletal disruption to promote vesicle formation. eMigrasome biogenesis depends on core migrasome machinery and recapitulates the biophysical and molecular features of native migrasomes while achieving higher production efficiency. In murine models, eMigrasomes loaded with a model antigen elicited potent antibody responses and retained structural integrity and immunogenicity at room temperature. Moreover, eMigrasomes displaying the SARS-CoV-2 Spike protein induced strong humoral responses and conferred protection against viral challenge in mice. These results establish eMigrasomes as an innovative, thermally stable, and broadly applicable vaccine platform derived from migrasome biology.
    Keywords:  cell biology; engineered migrasome; hypotonic shock; immunology; inflammation; mouse; vaccine
    DOI:  https://doi.org/10.7554/eLife.97621
  4. J Transl Med. 2025 Nov 11. 23(1): 1260
       BACKGROUND: Peripheral nerve injury (PNI) is a major clinical challenge with limited effective therapeutic options. Our prior work has demonstrated that SJMHE1, a peptide derived from Schistosoma japonicum, promotes peripheral nerve regeneration by regulating M2 macrophages; however, its downstream molecular mechanisms remain unclear. Migrasomes are newly identified migration-dependent extracellular vesicles that mediate intercellular communication, and are abundantly produced by highly migratory macrophages. The present study investigates whether SJMHE1 promotes peripheral nerve regeneration through macrophage-derived migrasomes, with a focus on the role of these migrasomes in macrophage-Schwann cell crosstalk.
    METHODS: The formation of migrasomes was observed using an in vivo rat model of sciatic nerve transection injury and in vitro macrophage-Schwann cell co-culture systems. SJMHE1-induced macrophage-derived migrasomes (SM-M) were systematically characterized: transmission electron microscopy (TEM) for morphological analysis, nanoparticle tracking analysis (NTA) for size distribution, and Western blotting (WB) for detecting migrasome marker proteins (e.g., TSPAN4, PIGK). The regulatory effects of SM-M on Schwann cell function were evaluated using multiple approaches: CCK-8 and EdU assays to assess cell proliferation, Transwell assays to measure cell migration in vitro; and a rat sciatic nerve crush injury model to verify in vivo regenerative effects (via immunofluorescence staining for S100 and NF200). Additionally, miRNA sequencing was performed on SM-M to identify key miRNAs and subsequent bioinformatics analysis was conducted to elucidate the potential molecular mechanisms by which SM-M regulates Schwann cell function.
    RESULTS: SJMHE1 treatment significantly enhances migrasome production in macrophages under both the in vivo and in vitro conditions. Functional experiments revealed that SM-M improve Schwann cell function in vivo and significantly promote the proliferation and migration of Schwann cells in vitro. Mechanistically, SM-M deliver miR-26b-5p to directly target and inhibit PTEN expression, thereby activating the AKT signaling pathway to regulate Schwann cell proliferation and migration.
    CONCLUSION: Our findings reveal a novel mechanism by which SJMHE1 promotes peripheral nerve regeneration through macrophage-Schwann cell communication mediated by miRNA delivery via macrophage migrasomes. This study highlights SJMHE1 as a promising therapeutic peptide for PNI and indicates that targeting migrasome-mediated communication between macrophages and Schwann cells may represent a new therapeutic strategy for PNI.
    Keywords:   Schistosoma japonicum peptide; Macrophages; Migrasome; Peripheral nerve regeneration; SJMHE1; Schwann cells; miR-26b-5p
    DOI:  https://doi.org/10.1186/s12967-025-07328-y
  5. Comput Biol Chem. 2025 Nov 06. pii: S1476-9271(25)00426-8. [Epub ahead of print]120(Pt 1): 108764
      The clinical presentation and inflammatory responses of acute respiratory distress syndrome (ARDS) had been previously described, yet the molecular mechanisms through which neutrophil migration occurs in such a condition were still unclear, hindering targeted therapeutic development. In the present study, we downloaded single-cell transcriptomic data of ARDS in the Gene Expression Omnibus (GEO) and calculated the migratory single-cell proportion on the basis of the single-sample Gene Set Enrichment Analysis (ssGSEA) approach. This method enabled us to find 1268 differentially expressed genes which are connected with migrasomes concerning neutrophils in ARDS. Incorporating LASSO and SVM-RFE models we also identified important genes, notably COMT, PTPRC, and RPAP2. Functional enrichment analysis, cell communication analysis through Cellcall and other bioinformatics tools including GSEA, GSVA, immune infiltration analysis, motif analysis, non-coding RNA analysis, and drug prediction were utilized to understand the molecular mechanism and find potential therapeutic targets of ARDS. Moreover, we verified the single-cell expression of the key genes, studied how and at what time they are co-expressed in tandem with the migration-related genes, and did a pseudo-temporal analysis of neutrophils. These key genes were identified as being associated with many pathways and the infiltration of immune cells. Mechanically, these genes can affect the movement of the neutrophils and ARDS. To conclude, our results indicate that migrasome-related mechanisms in neutrophils is also closely linked to ARDS progression, and parameters found by us, including genes like COMT, PTPRC, RPAP2 might be potential targets in treating ARDS in future.
    Keywords:  ARDS; Migrasomes; Neutrophils; Single-cell RNA sequencing; Therapeutic targets; Transcriptomics
    DOI:  https://doi.org/10.1016/j.compbiolchem.2025.108764