ArticleJournal of neuroinflammation2022
The primary macrophage chemokine, CCL2, is not necessary after a peripheral nerve injury for macrophage recruitment and activation or for conditioning lesion enhanced peripheral regeneration.
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 15 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Research hotspots and emerging trends of macrophages in peripheral nerve injury: a bibliometric and visualization analysis.Frontiers in cellular neuroscience · 2026Pooled it
- Revisiting the Peripheral Nerve Injury and Regeneration.Neuromolecular medicine · 2026Review
- Chemokine CCL2 Mediates Neuroglial Crosstalk and Drives Chronic Pain Pathogenesis.Neuroscience bulletin · 2025Review
- IGFBP2-Ceramide Pathway Mediates Divergent Myelin Breakdown in the PNS and CNS Following Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Carrier rocket-inspired hydrogel microspheres targeting subchondral bone osteoclast activity alleviate osteoarthritic pain and cartilage degeneration.Journal of nanobiotechnology · 2025Article
- The Dance Between Schwann Cells and Macrophages During the Repair of Peripheral Nerve Injury.Neuroscience bulletin · 2025Review
- The dual roles of chemokines in peripheral nerve injury and repair.Inflammation and regeneration · 2025Review
- Low-Intensity Pulsed Ultrasound: A Physical Stimulus with Immunomodulatory and Anti-inflammatory Potential.Annals of biomedical engineering · 2024Review
- Neither injury induced macrophages within the nerve, nor the environment created by Wallerian degeneration is necessary for enhanced in vivo axon regeneration after peripheral nerve injury.Journal of neuroinflammation · 2024Article
- Influence of Magnesium Degradation on Schwannoma Cell Responses to Nerve Injury Using an In Vitro Injury Model.Journal of functional biomaterials · 2024Article
- Modulation of central synapse remodeling after remote peripheral injuries by the CCL2-CCR2 axis and microglia.Cell reports · 2024Article
- Inflammatory changes in the choroid plexus following subarachnoid hemorrhage: the role of innate immune receptors and inflammatory molecules.Frontiers in cellular neuroscience · 2024Article
- GEO data mining identifies potential immune-related genes in hypertrophic scar and verities in a rabbit model.Heliyon · 2023Article
- Article
- Progress in methods for evaluating Schwann cell myelination and axonal growth in peripheral nerve regeneration via scaffolds.Frontiers in bioengineering and biotechnology · 2023Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundPeripheral nerve injuries stimulate the regenerative capacity of injured neurons through a neuroimmune phenomenon termed the conditioning lesion (CL) response. This response depends on macrophage accumulation in affected dorsal root ganglia (DRGs) and peripheral nerves. The macrophage chemokine CCL2 is upregulated after injury and is allegedly required for stimulating macrophage recruitment and pro-regenerative signaling through its receptor, CCR2. In these tissues, CCL2 is putatively produced by neurons in the DRG and Schwann cells in the distal nerve.
methodsCcl2
resultsSurprisingly, in all CKOs, DRG Ccl2 gene expression was decreased, while nerve Ccl2 was not. CCL2-RFP reporter mice revealed CCL2 expression in several cell types beyond the expected neurons and Schwann cells. Furthermore, macrophage accumulation, myelin clearance, and in vivo regeneration were unaffected in all CKOs, suggesting CCL2 may not be necessary for the CL response. Indeed, Ccl2 global knockout mice showed normal macrophage accumulation, myelin clearance, and in vivo regeneration, indicating these responses do not require CCL2. CCR2 ligands, Ccl7 and Ccl12, were upregulated after nerve injury and perhaps could compensate for the absence of Ccl2. Finally, Ccr2
conclusionsCCL2 is not necessary for macrophage accumulation, myelin clearance, and axon regeneration in the peripheral nervous system. Without CCL2, other CCR2 chemokines, resident macrophage proliferation, and CCR2-independent monocyte recruitment can compensate and allow for normal macrophage accumulation.
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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.