Mitochondrial heat shock protein 60 is increased in cerebrospinal fluid following pediatric traumatic brain injury

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Yichen Lai1, Christopher Stange, Stephen R Wisniewski

  • 1Department of Critical Care Medicine, Safar Center for Resuscitation Research, University of Pittsburgh School of Medicine, and Children's Hospital of Pittsburgh, PA 15213, USA.

Developmental Neuroscience
|September 1, 2006
PubMed

Insights

Elevated heat shock protein 60 (hsp60) in cerebrospinal fluid (CSF) indicates mitochondrial stress after traumatic brain injury (TBI). Higher hsp60 levels correlate with injury severity in children.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Cellular Biology

Background:

  • Traumatic brain injury (TBI) leads to mitochondrial dysfunction and cell death.
  • Heat shock protein 60 (hsp60), a mitochondrial protein, plays a role in cellular homeostasis.
  • Hsp60 induction in cerebral ischemia suggests a response to mitochondrial stress.

Purpose of the Study:

  • To measure hsp60 concentration in cerebrospinal fluid (CSF) after severe TBI in pediatric patients.
  • To investigate the association between CSF hsp60 levels and injury severity.

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) was used to quantify hsp60 in CSF.
  • CSF samples were collected from 34 pediatric TBI patients and 7 controls.
  • Glasgow Coma Scale (GCS) scores were used to define injury severity.

Main Results:

  • Peak CSF hsp60 concentration was significantly higher in TBI patients compared to controls (0.84 ng/ml vs. 0.0 ng/ml).
  • Hsp60 induction was observed early after TBI.
  • Peak hsp60 levels were independently associated with lower admission GCS scores, indicating greater injury severity.

Conclusions:

  • Increased CSF hsp60 levels may serve as a biomarker for early mitochondrial stress or damage following TBI in children.
  • Hsp60 elevation correlates with the severity of traumatic brain injury.

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