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Cited by 61Traumatic Brain Injury and Neurovascular DisturbancesTraumatic Brain Injury ResearchCell death mechanisms and regulation

Evaluation of apoptosis in cerebrospinal fluid of patients with severe head injury

Uzan, M., Erman, H., Tanriverdi, T., Sanus, G. Z., Kafadar, A., Uzun, H.·2006·Acta Neurochirurgica
DOI 10.1007/s00701-006-0887-1
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Abstract

Objective To determine whether sFas, caspase-3, proteins which propagate apoptosis, and bcl-2, a protein which inhibits apoptosis, would be increased in cerebrospinal fluid (CSF) in patients with severe traumatic brain injury (TBI) and to examine the correlation of sFas, caspase-3, and bcl-2 with each other and with clinical variables.Methods sFas, caspase-3, and bcl-2 were measured in CSF of 14 patients with severe TBI on days 1, 2, 3, 5, 7, and 10 post-trauma. The results were compared with CSF samples from control patients who had no brain and spinal pathology and had undergone spinal anesthesia for some other reason. Soluble Fas and bcl-2 were measured by ELISA while caspase-3 was measured enzymatically.Results No sFas, caspase-3, and bcl-2 activities were found in CSF of controls, but activities significantly increased in CSF of patients at all time points post-trauma (p < 0.01). Caspase-3 significantly correlated to intracranial pressure (p = 0.01) and cerebral perfusion pressure (p = 0.04). Soluble Fas and caspase-3 peaks coincided on day 5 post-trauma and there was significant association between sFas and caspase-3 increase (p = 0.01).Conclusion This study indicates a prolonged activation of pro-apoptotic (sFas, caspase-3) and anti-apoptotic (bcl-2) proteins after severe TBI in humans. The degree of activation of particularly caspase-3 may be related to the severity of the injury. Parallel increases of these three molecules may indicate a pivotal role of apoptosis in the pathophysiology of post-traumatic brain oedema, secondary cell destruction and chronic cell loss following severe TBI and may open new targets for post-traumatic therapeutic interventions.

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  • The above-mentioned events lead to membrane degradation of cellular and vascular structures and eventually to necrosis or apoptosis of neurons.

    “Furthermore, the above-mentioned events lead to membrane degradation of the cellular and vascular structures and eventually to necrosis or apoptosis of neurons (97,129,130).”

    From Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach (2015) · cites this paper as [130]

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Authors
Uzan, M., Erman, H., Tanriverdi, T., Sanus, G. Z., Kafadar, A., & Uzun, H.
Affiliations
Istanbul University-Cerrahpaşa (TR)
ORCID
Venue
Acta Neurochirurgica
Publisher
Springer Science and Business Media LLC
Published
2006-09-14
Volume
148
Issue
11
Pages
1157-1164
ISSN
  • 0001-6268 (ISSN-L)
  • 0942-0940
DOI
10.1007/s00701-006-0887-1
OpenAlex
W1980588653
Cited by
61
References
39
Citations by year
2025: 1 · 2024: 2 · 2023: 2 · 2022: 3 · 2021: 7 · 2020: 7 · 2019: 3 · 2018: 4 · 2017: 6 · 2016: 1 · 2015: 6 · 2014: 2 · 2013: 1 · 2012: 1
FWCI
0.93
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Acta Neurochirurgica (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
  • Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
apoptosis, cerebrospinal fluid biomarkers, severe traumatic brain injury, soluble Fas, caspase-3, Bcl-2, intracranial pressure, cerebral perfusion pressure, secondary cell death, injury severity
MeSH terms
Adolescent, Adult, Aged, Brain Injuries, Child, Child, Preschool, Enzyme Activation, Female, Humans, Male, Nerve Degeneration, Predictive Value of Tests, Biomarkers, Up-Regulation, Apoptosis, fas Receptor, Proto-Oncogene Proteins c-bcl-2, Apoptosis Regulatory Proteins, Caspase 3

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