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Hazeldine J, Dinsdale RJ, Naumann DN, et al. Traumatic injury is associated with reduced deoxyribonuclease activity and dysregulation of the actin scavenging system. Burns Trauma. 2021;9:tkab001doi: 10.1093/burnst/tkab001.
Hazeldine, J., Dinsdale, R. J., Naumann, D. N., Acharjee, A., Bishop, J. R. B., Lord, J. M., & Harrison, P. (2021). Traumatic injury is associated with reduced deoxyribonuclease activity and dysregulation of the actin scavenging system. Burns & trauma, 9tkab001. https://doi.org/10.1093/burnst/tkab001
Hazeldine, Jon, et al. "Traumatic injury is associated with reduced deoxyribonuclease activity and dysregulation of the actin scavenging system." Burns & trauma vol. 9 (2021): tkab001. doi: https://doi.org/10.1093/burnst/tkab001
Hazeldine J, Dinsdale RJ, Naumann DN, Acharjee A, Bishop JRB, Lord JM, Harrison P. Traumatic injury is associated with reduced deoxyribonuclease activity and dysregulation of the actin scavenging system. Burns Trauma. 2021 Apr 01;9:tkab001. doi: 10.1093/burnst/tkab001. eCollection 2021 Jan. PMID: 33834079; PMCID: PMC8014516.
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Burns Trauma. 2021 Apr 01;9:tkab001. doi: 10.1093/burnst/tkab001. eCollection 2021 Jan.

Traumatic injury is associated with reduced deoxyribonuclease activity and dysregulation of the actin scavenging system.

Burns & trauma

Jon Hazeldine, Robert J Dinsdale, David N Naumann, Animesh Acharjee, Jonathan R B Bishop, Janet M Lord, Paul Harrison

Affiliations

  1. Institute of Inflammation and Ageing, University of Birmingham, Edgbaston, Birmingham, West Midlands, B15 2TT, United Kingdom.
  2. National Institute for Health Research Surgical Reconstruction and Microbiology Research Centre, Heritage Building, Queen Elizabeth Hospital Birmingham, Mindelsohn Way, Edgbaston, Birmingham, West Midlands, B15 2TH, United Kingdom.
  3. Scar Free Foundation Birmingham Centre for Burns Research, University Hospital Birmingham Foundation Trust, Queen Elizabeth Hospital Birmingham, Mindelsohn Way, Edgbaston, Birmingham, West Midlands, B15 2TH, United Kingdom.
  4. Academic Department of Military Surgery and Trauma, Royal Centre for Defence Medicine, Queen Elizabeth Hospital Birmingham, Mindelsohn Way, Edgbaston, Birmingham, West Midlands, B15 2TH, United Kingdom.
  5. Institute of Cancer and Genomic Sciences, Centre for Computational Biology, University of Birmingham, Edgbaston, Birmingham, West Midlands, B15 2TT, United Kingdom.

PMID: 33834079 PMCID: PMC8014516 DOI: 10.1093/burnst/tkab001

Abstract

BACKGROUND: Traumatic injury is associated with increased concentrations of cell-free DNA (cfDNA) in the circulation, which contribute to post-injury complications. The endonuclease deoxyribonuclease 1 (DNase-1) is responsible for removing 90% of circulating cfDNA. Recently, DNase activity was reported to be significantly reduced following major non-traumatic brain injury (TBI), but the processes responsible were not investigated. Moreover, it is not known how quickly following injury DNase activity is reduced and whether this also occurs after TBI.

METHODS: At 3 post-injury time points (≤1, 4-12 and 48-72 hours), blood samples were obtained from 155 adult trauma patients that had sustained an isolated TBI (n = 21), TBI with accompanying extracranial injury (TBI

RESULTS: Significantly elevated concentrations of plasma cfDNA were seen in TBI, TBI

CONCLUSIONS: The post-traumatic increase in circulating cfDNA that occurs following extracranial trauma and TBI is accompanied by reduced DNase activity. We propose that, secondary to reduced GSN and VDBP levels, elevated circulating concentrations of G-actin underlie the post-injury reduction in DNase activity. Reducing circulating cfDNA levels via therapeutic restoration of DNase-1 activity may improve clinical outcomes post-injury.

© The Author(s) 2021. Published by Oxford University Press.

Keywords: Cell-free DNA; Deoxyribonuclease; Extracellular actin scavenging system; Pre-hospital; Trauma

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