Macrophages Driving Heterotopic Ossification: Convergence of Genetically-Driven and Trauma-Driven Mechanisms (original) (raw)

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Identification of Two Distinct Macrophage Subsets with Divergent Effects Causing either Neurotoxicity or Regeneration in the Injured Mouse Spinal Cord

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Mast cells protect from post-traumatic spinal cord damage in mice by degrading inflammation-associated cytokines via mouse mast cell protease 4

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Acute injury in the peripheral nervous system triggers an alternative macrophage response

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Traumatic brain injury induces macrophage subsets in the brain

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Infiltrating Blood-Derived Macrophages Are Vital Cells Playing an Anti-inflammatory Role in Recovery from Spinal Cord Injury in Mice

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Depletion of macrophages reduces axonal degeneration and hyperalgesia following nerve injury

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Macrophage-derived oncostatin M contributes to human and mouse neurogenic heterotopic ossifications

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Lesion-Induced Changes in the Production of Newly Synthesized and Secreted Apo-E and Other Molecules Are Independent of the Concomitant Recruitment of Blood-Borne Macrophages into Injured Peripheral Nerves

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Macrophage/microglia activation factor expression is restricted to lesion-associated microglial cells after brain trauma

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Macrophage Response to Peripheral Nerve Injury: The Quantitative Contribution of Resident and Hematogenous Macrophages

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Osteopontin-Deficient Mice Exhibit Less Inflammation, Greater Tissue Damage, and Impaired Locomotor Recovery from Spinal Cord Injury Compared with Wild-Type Controls

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Brain trauma elicits non-canonical macrophage activation states

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Inhibition of Posttraumatic Microglial Proliferation in a Genetic Model of Macrophage Colony-Stimulating Factor Deficiency in the Mouse

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Rapid Response of Identified Resident Endoneurial Macrophages to Nerve Injury

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Macrophagic and microglial responses after focal traumatic brain injury in the female rat

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Hematogenous macrophage depletion reduces the fibrotic scar and increases axonal growth after spinal cord injury

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Neurogenic Heterotopic Ossifications Develop Independently of Granulocyte Colony‐Stimulating Factor and Neutrophils

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