ArticleJournal of neuroinflammation2023
Endothelial progenitor cell-derived exosomes promote anti-inflammatory macrophages via SOCS3/JAK2/STAT3 axis and improve the outcome of spinal cord injury.
Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Bibliometric analysis of nanotechnology in spinal cord injury: current status and emerging frontiers.Frontiers in pharmacology · 2024Pooled it
- The Role and Mechanism of Endothelial Progenitor Cell-Derived Extracellular Vesicles in Vascular Repair of Ischemic Heart Disease.Journal of cardiovascular translational research · 2026Review
- Exosomal PSMD1 Derived From Dental Pulp Mesenchymal Stem Cells Promotes Microglial M2 Polarization to Alleviate Spinal Cord Injury.CNS neuroscience & therapeutics · 2026Article
- M2 polarization of macrophages: Manipulation of spinal cord injury repair.Neural regeneration research · 2026Article
- Neonatal small extracellular vesicle-loaded GelNB hydrogel reprograms the vascular-immune microenvironment for spinal cord injury repair.Bioactive materials · 2026Article
- Endothelial progenitor cells-derived exosomes reduce ferroptosis and promote neovascularization after intracranial atherosclerosis in association with the NCOA4/FTH1 cascade modulation.Drug delivery and translational research · 2026Article
- STAT3 Signaling in Spinal Cord Injury: Neurochemical Mechanisms Linking Neuroinflammation, Mitochondrial Stress, and Glial Remodeling.Neurochemical research · 2026Review
- Beta-Glucan modulates monocyte plasticity and differentiation capacity to mitigate DSS-induced colitis.eLife · 2026Article
- Decidual macrophage-mediated ferroptosis in trophoblasts leads to recurrent spontaneous abortion.iMeta · 2026Article
- Slfn4-mediated Stat3 signaling promotes suppressive bone marrow monocytes in a murine second-hit sepsis model.Molecular medicine (Cambridge, Mass.) · 2026Article
- A review of recent advances in exosome-mediated drug delivery for regenerative therapy and immunomodulation.Biomedical engineering online · 2026Review
- Research Progress on Spinal Cord Repair Based on Regulation of the Neuroregenerative Microenvironment.Cellular and molecular neurobiology · 2026Review
- From Cerebrovascular Injury to Vascular Cognitive Impairment and Dementia: Therapeutic Potential of Stem Cell-Derived Extracellular Vesicles.Biomedicines · 2026Review
- Exosome-derived ncRNAs and proteins: inflammation regulatory mechanisms and biomarker potential in spinal cord injury.Frontiers in molecular biosciences · 2026Review
- Extracellular vesicle-based therapeutic strategies for spinal cord injury.Extracellular vesicles and circulating nucleic acids · 2026Review
- Pancreatic Elastase Affects Liver Injury by Activating Proinflammatory Cytokines in Kupffer Cells via the JAK2/STAT3 Signaling Pathway.Current molecular medicine · 2026Article
- Exosomes as regenerative therapeutics for spinal cord injury: mechanisms and clinical prospects.Frontiers in medicine · 2026Review
- Mammalian, plant, and gut microbiota-derived extracellular vesicles as emerging therapeutics for bone diseases.Frontiers in bioengineering and biotechnology · 2026Review
- Nanoscale Delivery of MicroRNAs via Extracellular Vesicles: Mechanisms Potential in Modulating Cellular Senescence.International journal of nanomedicine · 2026Review
- Cyanobacteria-Derived Extracellular Vesicles: A Novel Frontier in Drug Delivery and Therapeutics.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundMacrophage in the spinal cord injury (SCI) area imparts a chronic pro-inflammation effect that challenges the recovery of SCI. Previously, endothelial progenitor cell-produced exosomes (EPC-EXOs) have been noticed to facilitate revascularization and inflammation control after SCI. However, their effects on macrophage polarization remained unclear. This study aimed to investigate the EPC-EXOs' role in macrophage polarization and reveal its underlying mechanism.
methodsWe extracted the macrophages and EPC from the bone marrow suspension of C57BL/L mice by centrifugation. After cell identification, the EPC-EXOs were collected by ultra-high-speed centrifugation and exosome extraction kits and identified by transmission electron microscopy and nanoparticle tracking analysis. Then, macrophages were cultured with EPC-EXOs in different concentrations. We labeled the exosome to confirm its internalization by macrophage and detected the macrophage polarization marker level both in vitro and in vivo. We further estimated EPC-EXOs' protective effects on SCI by mice spinal cord tissue H&E staining and motor behavior evaluation. Finally, we performed RT-qPCR to identify the upregulated miRNA in EPC-EXOs and manipulate its expression to estimate its role in macrophage polarization, SOCS3/JAK2/STAT3 pathway activation, and motor behavior improvement.
resultsWe found that EPC-EXOs decreased the macrophages' pro-inflammatory marker expression and increased their anti-inflammatory marker expression on the 7 and 14 days after SCI. The spinal cord H&E staining results showed that EPC-EXOs raised the tissue-sparing area rate significantly after 28 days of SCI and the motor behavior evaluation indicated an increased BMS score and motor-evoked potential by EPC-EXOs treatment after SCI. The RT-qPCR assay identified that miR-222-3P upregulated in EPC-EXOs and its miRNA-mimic also decreased the pro-inflammatory macrophages and increased the anti-inflammatory macrophages. Additionally, miR-222-3P mimic activated the SOCS3/JAK2/STAT3 pathway, and SOCS3/JAK2/STAT3 pathway inhibition blocked miR-2223P's effects on macrophage polarization and mouse motor behavior.
conclusionComprehensively, we discovered that EPC-EXOs-derived miR-222-3p affected macrophage polarization via SOCS3/JAK2/STAT3 pathway and promoted mouse functional repair after SCI, which reveals EPC-EXOs' role in modulation of macrophage phenotype and will provide a novel interventional strategy to induce post-SCI recovery.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.