The DOI matches its Crossref record; 60 of the 60 references it cites were found in a registry or an index.
High-resolution intravital imaging reveals that blood-derived macrophages but not resident microglia facilitate secondary axonal dieback in traumatic spinal cord injury
Abstract
After traumatic spinal cord injury, functional deficits increase as axons die back from the center of the lesion and the glial scar forms. Axonal dieback occurs in two phases: an initial axon intrinsic stage that occurs over the first several hours and a secondary phase which takes place over the first few weeks after injury. Here, we examine the secondary phase, which is marked by infiltration of macrophages. Using powerful time-lapse multi-photon imaging, we captured images of interactions between Cx3cr1(+/GFP) macrophages and microglia and Thy-1(YFP) axons in a mouse dorsal column crush spinal cord injury model. Over the first few weeks after injury, axonal retraction bulbs within the lesion are static except when axonal fragments are lost by a blebbing mechanism in response to physical contact followed by phagocytosis by mobile Cx3Cr1(+/GFP) cells. Utilizing a radiation chimera model to distinguish marrow-derived cells from radio-resistant CNS-resident microglia, we determined that the vast majority of accumulated cells in the lesion are derived from the blood and only these are associated with axonal damage. Interestingly, CNS-resident Cx3Cr1(+/GFP) microglia did not increasingly accumulate nor participate in neuronal destruction in the lesion during this time period. Additionally, we found that the blood-derived cells consisted mainly of singly labeled Ccr2(+/RFP) macrophages, singly labeled Cx3Cr1(+/GFP) macrophages and a small population of double-labeled cells. Since all axon destructive events were seen in contact with a Cx3Cr1(+/GFP) cell, we infer that the CCR2 single positive subset is likely not robustly involved in axonal dieback. Finally, in our model, deletion of CCR2, a chemokine receptor, did not alter the position of axons after dieback. Understanding the in vivo cellular interactions involved in secondary axonal injury may lead to clinical treatment candidates involving modulation of destructive infiltrating blood monocytes.
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“Given that peripheral monocytes have been shown to participate in CNS disease via both infiltration and repopulation of neuroglia following microglia depletion (4–10), it is important to determine if CSF1R inhibition causes functional changes in peripheral immune cells that can become part of the CNS (3, 4, 10–14).”
From CSF1R inhibition by a small-molecule inhibitor is not microglia specific; affecting hematopoiesis and the function of macrophages (2020) · cites this paper as [5]
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Metadata
- Authors
- Evans, T. A., Barkauskas, D. S., Myers, J. T., Hare, E. G., You, J. Q., Ransohoff, R. M., Huang, A. Y., & Silver, J.
- Venue
- Experimental Neurology
- Publisher
- Elsevier BV
- Published
- 2014-04
- Volume
- 254
- Pages
- 109-120
- ISSN
- 0014-4886
- PMC
- PMC3954731
- Cited by
- 181
- References
- 60
- Language
- en
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- creativecommons.org/licenses/by-nc-nd/3.0/ (vor)
- Funders
- MSTP (T32 GM007250, 5T32EB7509)
- NINDS (R01 NS25713)
- NCI (R01 CA154656)
- Dana Foundation
- St. Baldrick's Foundation
- Alex's Lemonade Stand Foundation
- Gabrielle's Angel Foundation
- Hyundai Hope-on-Wheels Research Program
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