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ABSTRACT: Circulating endothelial progenitor cells (EPCs) play an important role in angiogenesis and vasculogenesis. Statins administered promote functional improvement in rats, independent of their capability to lower cholesterol. Whether statin treatment regulates circulating EPCs after traumatic brain injury (TBI) has not been investigated. We hypothesized that atorvastatin increases circulating EPCs and promotes angiogenesis in TBI rats. Wistar rats (20 months old) were subjected to TBI and treated with or without atorvastatin (orally administered, 1mg/kg/day) starting 1h after TBI and then daily for 14 consecutive days. Long term potentiation (LTP) in the cornu ammonis1 of the hippocampus as well as the Modified Neurological Severity Score (mNSS) and the Morris Water Maze (MWM) functional tests were performed. Blood circulating EPCs were identified by flow cytometry. Rats were sacrificed 25 days after TBI. vWF and CD31 immunostaining was performed. We found that atorvastatin administration significantly induced angiogenesis and increased circulating EPC levels as well as improved functional recovery when compared with non-treatment TBI-control rats (P<0.05). The circulating EPC level is correlated with vascular density (r=0.878, P <0.05) and CD31 positive cell number in the injured brain (r=0.921, P <0.05). The results suggest that increasing circulating EPCs with atorvastatin treatment may contribute to the observed increase in angiogenesis and improved functional outcome after TBI.
Journal of the neurological sciences 06/2012; 319(1-2):117-23. · 2.32 Impact Factor
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Huijie Wei,
Qun Mao,
Li Liu,
Yong Xu,
Jieli Chen,
Rongcai Jiang,
Long Yin,
Yimu Fan,
Michael Chopp,
Jingfei Dong,
Jianning Zhang
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ABSTRACT: Endothelial dysfunction is a trigger for the formation of cerebral aneurysm (CA). The circulating endothelial progenitor cell (EPC) plays an important role in postnatal vasculogenesis and reduction of endothelial injury. In this study, we tested the hypothesis that decreased number and impaired function of circulating EPCs correlate with CA formation in patients. Blood circulating EPCs were identified by flow cytometry. The level of plasma vascular endothelial growth factor (VEGF) was measured by ELISA. Circulating EPCs from patients (n = 27) were cultured in vitro, and the function of EPCs was evaluated by cell migration and senescence-associated β-galactosidase activity. The number of circulating EPCs was significantly decreased in both unruptured and ruptured CA patients compared with healthy control subjects. Impaired migratory capacity and elevated cellular senescence of cultured EPCs were observed in patients with CA (ruptured and unruptured). The percentages of EPC senescence in patients with CAs were significantly and negatively correlated with the number of circulating EPCs. In addition, there were higher levels of plasma VEGF in CA patients compared with healthy control subjects. Our results show that the numbers and functions of circulating EPCs are reduced in patients with CAs. These findings suggest that the decreased number and impaired function of circulating EPCs in CA patients may contribute to the pathophysiological process of aneurysm formation.
Journal of Neuroscience Research 07/2011; 89(11):1822-8. · 2.74 Impact Factor
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ABSTRACT: Vascular remodeling plays a key role in neural regeneration in the injured brain. Circulating endothelial progenitor cells (EPCs) are a mediator of the vascular remodeling process. Previous studies have found that progesterone treatment of traumatic brain injury (TBI) decreases cerebral edema and cellular apoptosis and inhibits inflammation, which in concert promote neuroprotective effects in young adult rats. However, whether progesterone treatment regulates circulating EPC level and fosters vascular remodeling after TBI have not been investigated. In this study, we hypothesize that progesterone treatment following TBI increases circulating EPC levels and promotes vascular remodeling in the injured brain in aged rats. Male Wistar 20-month-old rats were subjected to a moderate unilateral parietal cortical contusion injury and were treated with or without progesterone (n=54/group). Progesterone was administered intraperitoneally at a dose of 16mg/kg at 1 h post-TBI and was subsequently injected subcutaneously daily for 14 days. Neurological functional tests and immnunostaining were performed. Circulating EPCs were measured by flow cytometry. Progesterone treatment significantly improved neurological outcome after TBI measured by the modified neurological severity score, Morris Water Maze and the long term potentiation in the hippocampus as well as increased the circulating EPC levels compared to TBI controls (p<0.05). Progesterone treatment also significantly increased CD34 and CD31 positive cell number and vessel density in the injured brain compared to TBI controls (p<0.05). These data indicate that progesterone treatment of TBI improves multiple neurological functional outcomes, increases the circulating EPC level, and facilitates vascular remodeling in the injured brain after TBI in aged rats.
Journal of neurotrauma 05/2011; 29(2):343-53. · 4.25 Impact Factor
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ABSTRACT: 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.
None.
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.
Critical care medicine 03/2011; 39(7):1760-5. · 6.37 Impact Factor
