ArticleJournal of neurotrauma2010
Comparison of immunopathology and locomotor recovery in C57BL/6, BUB/BnJ, and NOD-SCID mice after contusion spinal cord injury.
Article in Journal of neurotrauma, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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
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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- C1q drives neural stem cell quiescence by regulating cell cycle and metabolism through BAI1.Nature communications · 2025Article
- Maladaptive changes in the homeostasis of AEA-TRPV1/CB1R induces pain-related hyperactivity of nociceptors after spinal cord injury.Cell & bioscience · 2025Article
- Enhanced oxidative phosphorylation, re-organized intracellular signaling, and epigenetic de-silencing as revealed by oligodendrocyte translatome analysis after contusive spinal cord injury.Scientific reports · 2023Article
- Restoring mitochondrial cardiolipin homeostasis reduces cell death and promotes recovery after spinal cord injury.Cell death & disease · 2022Article
- Single cell profiling of CD45Journal of neuroinflammation · 2022Article
- Sexual dimorphism in neurological function after SCI is associated with disrupted neuroinflammation in both injured spinal cord and brain.Brain, behavior, and immunity · 2022Article
- L-Arginine Depletion Improves Spinal Cord Injury via Immunomodulation and Nitric Oxide Reduction.Biomedicines · 2022Article
- Article
- Novel C1q receptor-mediated signaling controls neural stem cell behavior and neurorepair.eLife · 2020Article
- Reaching and Grasping Training Improves Functional Recovery After Chronic Cervical Spinal Cord Injury.Frontiers in cellular neuroscience · 2020Article
- Unbiased transcriptomic analyses reveal distinct effects of immune deficiency in CNS function with and without injury.Protein & cell · 2019Article
- Innovative mouse model mimicking human-like features of spinal cord injury: efficacy of Docosahexaenoic acid on acute and chronic phases.Scientific reports · 2019Article
- A biodegradable hybrid inorganic nanoscaffold for advanced stem cell therapy.Nature communications · 2018Article
- The Biology of Regeneration Failure and Success After Spinal Cord Injury.Physiological reviews · 2018Review
- The Effects of Icariin on Enhancing Motor Recovery Through Attenuating Pro-inflammatory Factors and Oxidative Stress via Mitochondrial Apoptotic Pathway in the Mice Model of Spinal Cord Injury.Frontiers in physiology · 2018Article
- Systemic Neutrophil Depletion Modulates the Migration and Fate of Transplanted Human Neural Stem Cells to Rescue Functional Repair.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Neutrophils Induce Astroglial Differentiation and Migration of Human Neural Stem Cells via C1q and C3a Synthesis.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Hormonal therapy in traumatic spinal cord injury.American journal of translational research · 2017Review
- miR-155 Deletion in Mice Overcomes Neuron-Intrinsic and Neuron-Extrinsic Barriers to Spinal Cord Repair.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Traumatic spinal cord injury in mice with human immune systems.Experimental neurology · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Studies of cell transplantation therapeutics in animal models of traumatic spinal cord injury (SCI) are often hampered by partial or complete rejection of the graft by the host. Pharmacological immunosuppression is rarely sufficient to prevent rejection. Further, the immunological niche created by both the host immune response and immunosuppressant drugs could hypothetically influence the proliferation, differentiation, and fate of transplanted progenitor/stem cells. To avoid these confounds, we have previously used the constitutively immunodeficient non-obese diabetic severe combined immunodeficient (NOD-SCID) mouse as a model for transplantation studies following SCI. In the current study, we compare behavioral and histological recovery in NOD-SCID, C57BL/6, and BUB/BnJ mice of both sexes to better facilitate interpretation of data from studies using NOD-SCID mice. Of the strains examined, NOD-SCID mice exhibited the greatest locomotor recovery in the open field; no sex differences were detected in locomotor recovery in any of the strains. Stereologic estimation of the number of infiltrated neutrophils showed more cells in C57BL/6 mice than NOD-SCID mice, with BUB/BnJ mice having an intermediate number. The volume of macrophages/microglia did not differ between strains or sexes, though more rostral-caudal spreading was observed in C57BL/6 and BUB/BnJ than NOD-SCID mice. No significant differences were detected in lesion volume. Taken together these findings demonstrate that relative to other strains, NOD-SCID mice have both similar primary lesion volume and cellular inflammatory parameters after SCI, and support the applicability of the model for neurotransplantation studies.
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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.