ArticleNeurobiology of disease2011
CD47 knockout mice exhibit improved recovery from spinal cord injury.
Article in Neurobiology of disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- Emerging role of neural stem/progenitor cell secretome in brain inflammatory response modulation.Pharmacological reports : PR · 2025Review
- The role of CD47 in non-neoplastic diseases.Heliyon · 2023Review
- CD47 in the Brain and Neurodegeneration: An Update on the Role in Neuroinflammatory Pathways.Molecules (Basel, Switzerland) · 2021Review
- Following spinal cord injury, PDE4B drives an acute, local inflammatory response and a chronic, systemic response exacerbated by gut dysbiosis and endotoxemia.Neurobiology of disease · 2019Article
- Deficiency in matrix metalloproteinase-2 results in long-term vascular instability and regression in the injured mouse spinal cord.Experimental neurology · 2016Article
- Physiological Capillary Regression is not Dependent on Reducing VEGF Expression.Microcirculation (New York, N.Y. : 1994) · 2016Review
- Inflammogenesis of Secondary Spinal Cord Injury.Frontiers in cellular neuroscience · 2016Review
- Interplay between Cellular and Molecular Inflammatory Mediators in Lung Cancer.Mediators of inflammation · 2016Review
- SIRP/CD47 signaling in neurological disorders.Brain research · 2015Review
- A murine toolbox for imaging the neurovascular unit.Microcirculation (New York, N.Y. : 1994) · 2015Review
- CD36 deletion improves recovery from spinal cord injury.Experimental neurology · 2014Article
- Acute and chronic mu opioids differentially regulate thrombospondins 1 and 2 isoforms in astrocytes.ACS chemical neuroscience · 2014Article
- microRNAs in spinal cord injury: potential roles and therapeutic implications.International journal of biological sciences · 2014Review
- Dorsal column sensory axons degenerate due to impaired microvascular perfusion after spinal cord injury in rats.Experimental neurology · 2013Article
- Degeneration of phrenic motor neurons induces long-term diaphragm deficits following mid-cervical spinal contusion in mice.Journal of neurotrauma · 2012Article
- Article
- The matricellular protein thrombospondin-1 globally regulates cardiovascular function and responses to stress via CD47.Matrix biology : journal of the International Society for Matrix Biology · 2012Review
- Thrombospondins as key regulators of synaptogenesis in the central nervous system.Matrix biology : journal of the International Society for Matrix Biology · 2012Review
- Sildenafil improves epicenter vascular perfusion but not hindlimb functional recovery after contusive spinal cord injury in mice.Journal of neurotrauma · 2012Article
- The absence of CD47 promotes nerve fiber growth from cultured ventral mesencephalic dopamine neurons.PloS one · 2012Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Recent data have implicated thrombospondin-1 (TSP-1) signaling in the acute neuropathological events that occur in microvascular endothelial cells (ECs) following spinal cord injury (SCI) (Benton et al., 2008b). We hypothesized that deletion of TSP-1 or its receptor CD47 would reduce these pathological events following SCI. CD47 is expressed in a variety of tissues, including vascular ECs and neutrophils. CD47 binds to TSP-1 and inhibits angiogenesis. CD47 also binds to the signal regulatory protein (SIRP)α and facilitates neutrophil diapedesis across ECs to sites of injury. After contusive SCI, TSP-1(-/-) mice did not show functional improvement compared to wildtype (WT) mice. CD47(-/-) mice, however, exhibited functional locomotor improvements and greater white matter sparing. Whereas targeted deletion of either CD47 or TSP-1 improved acute epicenter vascularity in contused mice, only CD47 deletion reduced neutrophil diapedesis and increased microvascular perfusion. An ex vivo model of the CNS microvasculature revealed that CD47(-/-)-derived microvessels (MVs) prominently exhibit adherent WT or CD47(-/-) neutrophils on the endothelial lumen, whereas WT-derived MVs do not. This implicates a defect in diapedesis mediated by the loss of CD47 expression on ECs. In vitro transmigration assays confirmed the role of SIRPα in neutrophil diapedesis through EC monolayers. We conclude that CD47 deletion modestly, but significantly, improves functional recovery from SCI via an increase in vascular patency and a reduction of SIRPα-mediated neutrophil diapedesis, rather than the abrogation of TSP-1-mediated anti-angiogenic signaling.
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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.