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Updated: Jan 7, 2026
Mouse Model of Pressure Ulcers After Spinal Cord Injury
Published on: March 9, 2019
Spinal Cord Injury Disrupts Inflammatory Signaling and Impairs Skin Wound Healing: Evidence from Two Models of
Jessica M Marbourg1,2, Christopher P Vadala1,2,3,4, Leah M Pyter5,6
1Center for Brain and Spinal Cord Repair, Wexner Medical Center at The Ohio State University, Columbus, Ohio, USA.
Abstract:
Traumatic spinal cord injury (SCI) increases the risk for skin complications, including the development of decubitus ulcers, that is, pressure sores. The mechanisms by which SCI adversely affects skin health are poorly understood. To better understand how SCI affects the normal progression of wound healing, two mouse models of cutaneous wound healing were used. Mice received a high-level (T3) SCI or sham injury (Lam) over the first week postinjury. Mice received standardized skin wounds on the dorsum below the injury level (punch biopsy or compression/ischemia wounds). Planimetric analysis revealed that wound closure was consistently delayed and impaired after SCI. Subsequent analyses of the expression of genes and proteins responsible for regulating cell migration and recruitment, particularly of neutrophils, were reduced in SCI mice as early as 1 day post-wounding. This impaired chemotactic signaling was associated with a corresponding decrease in neutrophil recruitment to the wounds of SCI mice. At later phases of healing, the expression of inflammatory genes and the accumulation of wound myeloid cells with an elevated capacity for arginine catabolism was enhanced in SCI mice relative to Lam. Overall, data in this report show that impaired wound closure in SCI mice is associated with early and prolonged disruption of the expression of genes and proteins needed to coordinate the sequential progression through all phases of wound healing. Consequently, skin wounds in SCI mice exhibit prolonged inflammation, characteristic of complicated wound healing. Thus, targeting signaling pathways during the inflammatory phase of healing of decubitus ulcers after SCI could improve wound closure and limit further complications.
Insights
Traumatic spinal cord injury (SCI) impairs wound healing, delaying closure and prolonging inflammation. Targeting early inflammatory signaling pathways may improve healing of pressure sores after SCI.
Area of Science:
- Wound Healing Research
- Neuroscience
- Dermatology
Background:
- Traumatic spinal cord injury (SCI) elevates the risk of skin complications like pressure sores.
- Mechanisms linking SCI to poor skin health and impaired wound healing are not well understood.
Purpose of the Study:
- To investigate how SCI affects the normal progression of cutaneous wound healing.
- To identify molecular and cellular changes contributing to delayed healing post-SCI.
Main Methods:
- Utilized two mouse models for cutaneous wound healing after high-level spinal cord injury (T3 SCI) or sham injury.
- Assessed wound closure using planimetric analysis and examined gene/protein expression related to cell migration and inflammation.
Main Results:
- SCI mice exhibited delayed and impaired wound closure compared to controls.
- Reduced expression of genes/proteins for cell migration and neutrophil recruitment was observed early post-wounding in SCI mice.
- Later phases showed enhanced inflammatory gene expression and myeloid cell accumulation with increased arginine catabolism in SCI wounds.
Conclusions:
- Impaired wound healing in SCI is linked to early and sustained disruption of gene/protein expression crucial for coordinated healing phases.
- SCI-induced wounds display prolonged inflammation, indicative of complicated healing.
- Targeting inflammatory signaling during the initial phase of pressure ulcer healing after SCI could enhance wound closure and prevent complications.
