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Updated: Mar 10, 2026
Electromagnetic Controlled Closed-Head Model of Mild Traumatic Brain Injury in Mice
Published on: September 28, 2022
CD47 deficiency improves neurological outcomes of traumatic brain injury in mice
Song Zhao1, Zhanyang Yu2, Yu Liu3
1Departments of Orthopedic and Neurosurgery, The First Bethune Hospital of Jilin University, Changchun, Jilin, China; Neuroprotection Research Laboratory, Departments of Neurology and Radiology, Massachusetts General Hospital, Harvard Medical School, 149 13th Street, Room 2401, Charlestown, MA 02129, USA.
Abstract:
CD47 is a receptor for signal-regulatory protein alpha (SIRPα) in self-recognition by the innate immune system, and a receptor of thrombospondin-1 (TSP-1) contributing to vascular impairment in response to stress. However, the roles of CD47 in traumatic brain injury (TBI) have not been investigated. In this study we aimed to test our hypothesis that CD47 mediates early neutrophil brain infiltration and late brain vascular remodeling after TBI. Mice were subjected to TBI using a controlled cortical impact (CCI) device. We examined early phase neutrophil infiltration, and late phase brain vessel density, pro-angiogenic markers VEGF and Ang-1 protein expression, neurological function deficits and lesion volumes for up to three weeks after TBI. Our results show that mice deficient in CD47 (CD47 Knockout) had significantly less brain neutrophil infiltration at 24h, upregulated VEGF expression in peri-lesion cortex at 7 and 14days, and increased blood vessel density at 21days after TBI, compared to wild type (WT) mice. CD47 knockout also significantly decreased sensorimotor function deficits and reduced brain lesion volume at 21days after TBI. We conclude that CD47 may play pathological roles in brain neutrophil infiltration, progression of brain tissue damage, impairment of cerebrovascular remodeling and functional recovery after TBI.
Insights
CD47 blockade reduces neutrophil infiltration and brain damage after traumatic brain injury (TBI). CD47 knockout mice showed improved vascular remodeling and functional recovery post-TBI.
Area of Science:
- Neuroscience
- Immunology
- Vascular Biology
Background:
- CD47 acts as a receptor for SIRPα in innate immunity and TSP-1, impacting vascular responses.
- The role of CD47 in traumatic brain injury (TBI) remains unexplored.
- CD47's involvement in neuroinflammation and post-TBI vascular remodeling is unknown.
Purpose of the Study:
- To investigate the role of CD47 in mediating neutrophil infiltration and vascular remodeling following TBI.
- To test the hypothesis that CD47 contributes to early neutrophil brain infiltration and late vascular changes post-TBI.
Main Methods:
- Traumatic brain injury (TBI) was induced in mice using a controlled cortical impact (CCI) model.
- Evaluated early neutrophil infiltration and late-phase vascular density, VEGF/Ang-1 expression, neurological function, and lesion volume up to 3 weeks post-TBI.
- Compared CD47 knockout (KO) mice with wild-type (WT) littermates.
Main Results:
- CD47 KO mice exhibited significantly reduced brain neutrophil infiltration at 24 hours post-TBI.
- Upregulated VEGF expression and increased blood vessel density were observed in CD47 KO mice at later time points (7-21 days).
- CD47 deficiency led to decreased sensorimotor deficits and smaller lesion volumes at 21 days post-TBI.
Conclusions:
- CD47 plays a pathological role in TBI by promoting neutrophil infiltration and exacerbating brain tissue damage.
- Targeting CD47 may improve cerebrovascular remodeling and functional recovery after TBI.
- CD47 inhibition represents a potential therapeutic strategy for mitigating TBI consequences.
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