ArticleStem cell research & therapy2025
Long non-coding RNA Malat1 modulates CXCR4 expression to regulate the interaction between induced neural stem cells and microglia following closed head injury.
Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Combination of Astragaloside IV and Tetramethylpyrazine Promotes Angiogenesis via the MALAT1-CXCL12/CXCR4 Axis in Brain Endothelial Cells After Ischemic Injury.Medical science monitor : international medical journal of experimental and clinical research · 2026Article
- Neural Stem/Progenitor Cells Regulate Neuroinflammation: Mechanisms and Therapeutic Applications in Neurological Diseases.International journal of molecular sciences · 2026Review
- Silencing MALAT1 represses pathological progression, inflammation, and vascular smooth muscle cell phenotype switching by regulating the SEMA3C-mediated Smad pathway in intracranial aneurysms.Frontiers in cellular neuroscience · 2026Article
- The novel functions of chemokines in lung cancer progression.Frontiers in immunology · 2025Review
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Authors and funding
10 authors.
Funding
Abstract
backgroundClosed head injury (CHI) provokes a prominent neuroinflammation that may lead to long-term health consequences. Microglia plays pivotal and complex roles in neuroinflammation-mediated neuronal insult and repair following CHI. We previously reported that induced neural stem cells (iNSCs) can block the effects of CXCL12/CXCR4 signaling on NF-κB activation in activated microglia by CXCR4 overexpression. Here we aim to uncover the mechanism of CXCR4 upregulation in iNSCs.
methodsWe performed bioinformatic analysis to detect the differentially expressed genes in iNSCs after co-cultured with LPS-activated microglia. Subsequently, we predicted the target genes and performed gain- and loss-of-functional studies, dualluciferase reporter, RNA immunoprecipitation, biotin-coupled miRNA pulldown, fluorescence in situ hybridization and cell transplantation assays to further elucidate the mechanism underlying the immunoregulatory effects of iNSCs. Student's t-test and one-way analysis of variance (ANOVA) with Tukey's post hoc test were used to determine statistical significance.
resultsOur results indicated that Malat1 could act as a sponge of miR-139-5p to modulate the expression of CXCR4 that exerted significant influence on the immunoregulatory effects of iNSCs on the secretion of CXCL12, TNF-α and IGF-1 by activated microglia. Furthermore, Malat1 inhibition blocked the immunoregulatory effects of iNSC grafts on microglial activation as well as neuroinflammation in the injured cortices of CHI mice. Interestingly, NF-κB activation in iNSCs augmented the immunoregulatory effects of iNSCs on microglial activation by activating the axis of Malat1/miR-139-5p/Cxcr4. Notably, we found that TNF-α secreted by activated microglia could bind to TNFR1 at the surface of iNSCs to trigger NF-κB activation in iNSCs.
conclusionsIn short, our findings reveal a novel role of Malat1 in the immunomodulatory effects of iNSCs on microglial activation, suggesting that transplanted iNSCs may self-perceive the changes of the activated state of microglia and thus make prudential regulation of the neuroinflammation following CHI.
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