ArticleJournal of neuroinflammation2022
SU16f inhibits fibrotic scar formation and facilitates axon regeneration and locomotor function recovery after spinal cord injury by blocking the PDGFRβ pathway.
Article in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 36 citations in OpenAlex.
- Spatiotemporal disarray of inflammatory microenvironment following spinal cord injury.Neural regeneration research · 2026Article
- Electrical stimulation and stem cell subdural implantation decrease microglia reactivity after spinal cord injury.Materials today. Bio · 2026Article
- Review
- Targeting the glial-fibrotic scar microenvironment after spinal cord injury: From integrated protection to systematic regulation of regenerative balance.Journal of orthopaedic translation · 2026Review
- Simulated closed-loop magnetic stimulation promotes function recovery and axonal regeneration in spinal cord injury.Communications biology · 2026Article
- TREM2 Facilitates Myelin Debris Clearance but Exacerbates Chronic Inflammation and Fibrosis After Spinal Cord Injury.CNS neuroscience & therapeutics · 2026Article
- Profibrotic macrophage-derived CXCL4 promotes pericyte-to-myofibroblast transition after spinal cord injury.Journal of orthopaedic translation · 2026Article
- Screening macrophage polarization genes in spinal cord injury as therapeutic targets.PloS one · 2026Article
- Astrocytic Sirt2-Mediated Delactylation Limits Blood-Spinal Cord Barrier Reconstruction after Spinal Cord Injury.Research (Washington, D.C.) · 2026Article
- Targeting the Jun-Irf8-CD36 axis attenuates fibrotic scar formation and promotes functional recovery after spinal cord injury.Burns & trauma · 2026Article
- Regulatory T cells attenuate astrogliosis via IL-10/STAT3/PKC/vimentin signaling and promote neurological recovery after spinal cord injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Photobiomodulation Reduces Fibrous Scar Formation After Spinal Cord Injury by Downregulating CXCL3 Expression in Macrophages.Molecular neurobiology · 2025Article
- Curcumin-loaded polydopamine nanoparticles-based antioxidant scaffold promote spinal cord repair though dural-regulation of macrophage polarization.Materials today. Bio · 2025Article
- Dynamic phosphorylation of Fascin-1 orchestrates microglial phagocytosis and neurological recovery after spinal cord injury.Journal of neuroinflammation · 2025Article
- Centripetal migration and prolonged retention of microglia promotes spinal cord injury repair.Journal of neuroinflammation · 2025Article
- Trehalose enhances macrophage autophagy to promote myelin debris clearance after spinal cord injury.Cell & bioscience · 2025Article
- Glycosylated lysosomal membrane protein promotes tissue repair after spinal cord injury by reducing iron deposition and ferroptosis in microglia.Scientific reports · 2025Article
- Biological engineering approaches for modulating the pathological microenvironment and promoting axonal regeneration after spinal cord injury.Frontiers in neuroscience · 2025Review
- Runx2 Suppresses Astrocyte Activation and Astroglial Scar Formation After Spinal Cord Injury in Mice.Molecular neurobiology · 2024Article
- Galectin-3 inhibition reduces fibrotic scarring and promotes functional recovery after spinal cord injury in mice.Cell & bioscience · 2024Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundExcessively deposited fibrotic scar after spinal cord injury (SCI) inhibits axon regeneration. It has been reported that platelet-derived growth factor receptor beta (PDGFRβ), as a marker of fibrotic scar-forming fibroblasts, can only be activated by platelet-derived growth factor (PDGF) B or PDGFD. However, whether the activation of the PDGFRβ pathway can mediate fibrotic scar formation after SCI remains unclear.
methodsA spinal cord compression injury mouse model was used. In situ injection of exogenous PDGFB or PDGFD in the spinal cord was used to specifically activate the PDGFRβ pathway in the uninjured spinal cord, while intrathecal injection of SU16f was used to specifically block the PDGFRβ pathway in the uninjured or injured spinal cord. Immunofluorescence staining was performed to explore the distributions and cell sources of PDGFB and PDGFD, and to evaluate astrocytic scar, fibrotic scar, inflammatory cells and axon regeneration after SCI. Basso Mouse Scale (BMS) and footprint analysis were performed to evaluate locomotor function recovery after SCI.
resultsWe found that the expression of PDGFD and PDGFB increased successively after SCI, and PDGFB was mainly secreted by astrocytes, while PDGFD was mainly secreted by macrophages/microglia and fibroblasts. In addition, in situ injection of exogenous PDGFB or PDGFD can lead to fibrosis in the uninjured spinal cord, while this profibrotic effect could be specifically blocked by the PDGFRβ inhibitor SU16f. We then treated the mice after SCI with SU16f and found the reduction of fibrotic scar, the interruption of scar boundary and the inhibition of lesion and inflammation, which promoted axon regeneration and locomotor function recovery after SCI.
conclusionsOur study demonstrates that activation of PDGFRβ pathway can directly induce fibrotic scar formation, and specific blocking of this pathway would contribute to the treatment of SCI.
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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.