Endothelial progenitor cells play an active role in vascular repair and revascularization of tissue damaged by traumatic, inflammatory, and ischemic injures. We correlate the changes in circulating endothelial progenitor cells with the severity of traumatic brain injury. The study is designed to investigate the endothelial progenitor cell mobilization after injury and a potential use of circulating endothelial progenitor cells as a prognostic marker for evaluating trauma severity and clinical outcomes.
A prospective cohort study conducted in two neurosurgical intensive care units of Tianjin Medical University General Hospital and Tianjin Huanhu Hospital (Tianjin, China).
Patients with traumatic brain injury and age- and gender-matched healthy controls.
Changes in the levels of circulating endothelial progenitor cells were monitored for up to 21 days in 84 patients with traumatic brain injury. Results were correlated with the clinical assessment of injury severity as determined by the Glasgow Coma Scale. The level of circulating endothelial progenitor cells was found to be suppressed 24–48 hrs after injury but rapidly increased, reaching the highest at days 5–7 post-trauma. Circulating endothelial progenitor cells in patients with improved Glasgow Coma Scale scores were significantly higher than those with deteriorated conditions and remained persistently low in patients who died of trauma.
The results suggest that the level of circulating endothelial progenitor cells correlates with the clinical severity and outcome of traumatic brain injury and may offer potential as a prognostic marker for traumatic brain injury. A long-term follow-up of these patients is ongoing.
From the Department of Neurosurgery (LL, HW, FC, JW, JZ), Tianjin Medical University General Hospital, Tianjin Neurological Institute; Key Laboratory of Post-trauma Neuro-repair and Regeneration in Central Nervous System, Ministry of Education; Tianjin Key Laboratory of Injuries, Variations and Regeneration of Nervous System, Tianjin, China; and Thrombosis Research Section (JFD), Department of Medicine, Baylor College of Medicine, Houston, TX.
Supported, in part, by grants 2005CB522600 (JZ) and 30772229 (JZ) from the Chinese Science Foundation (Beijing, China) and grant HL71895 (JFD) from the National Institutes of Health (Bethesda, MD).
LL and HW contributed equally to this work.
The authors have not disclosed any potential conflicts of interest.
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