Dynamic Changes of Vascular Endothelial Growth Factor and Angiopoietin-1 in Association With Circulating Endothelial Progenitor Cells After Severe Traumatic Brain Injury
ABSTRACT Vascular endothelial growth factor (VEGF) and angiopoietin-1 (Ang-1) can promote angiogenesis and vascular stability after brain injury. Circulating endothelial progenitor cells (EPCs) also play a crucial role in neovascularization and tissue repair after traumatic brain injury (TBI). We sought to compare the expression of VEGF and Ang-1 in serum and the circulating EPCs in patients after severe TBI with that of healthy control subjects.
We obtained peripheral blood and serum samples from 21 patients with severe TBI and 11 healthy control subjects. EPCs in blood samples from severe TBI patients and healthy controls were quantified by flow cytometry 1 day, 4 days, 7 days, 14 days, and 21 days after severe TBI. VEGF and Ang-1 were measured by enzyme linked immunosorbent assay at the same time points.
Compared with control subjects, circulating EPCs in patients with severe TBI decreased 4 days (p < 0.05), but increased 7 days and 14 days (p < 0.05) after TBI. VEGF increased significantly during the follow-up period (p < 0.05). Ang-1 increased gradually and reached peak at 7 days and 14 days after TBI. The circulating EPCs were significantly correlated with VEGF and Ang-1 at 7 days and 14 days after severe TBI.
Our results suggest that the increased VEGF and Ang-1 are closely related to increase in circulating EPCs in response to severe TBI, which may be needed for vascular repairs after severe TBI.
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ABSTRACT: ObjectiveTBI causes localized cerebral ischemia that, in turn, is accompanied by both changes in BBB permeability and recruitment of CD34(+) cells to the injured tissue. However, it remains unknown whether CD34(+) cell recruitment is linked to BBB permeability. This study is a preliminary investigation into possible correlations between CD34(+) cell recruitment and BBB permeability following TBI in a rat model. Methods Male SD rats were subjected to mild fluid percussion injury. BBB permeability was assessed by measuring extrinsic EB dye extravasation and endogenous EBA expression at days 1, 3, 5, 7, and 12 post injury. The number of CD34(+) cells in the damaged tissue was analyzed by immunohistochemistry at each time point. ResultsEB dye extravasation reached a peak at day 3 following TBI, while EBA expression displayed the reverse profile. Accumulation of CD34(+) cells in injured brain tissue was evident at five days post injury. It revealed a negative linear correlation between CD34(+) cell and BBB permeability. Conclusions The negative linear correlation between CD34(+) cell recruitment and BBB permeability following TBI provides a support for further study of CD34(+) cell transplantation for BBB repair after TBI.Microcirculation (New York, N.Y.: 1994) 06/2014; 21(8). DOI:10.1111/micc.12150 · 2.26 Impact Factor
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ABSTRACT: Amyotrophic lateral sclerosis (ALS) is a severe neurodegenerative disease with a complicated and poorly understood pathogenesis. Strong evidence indicates impairment of all neurovascular unit components including the blood-brain and blood-spinal cord barriers (BBB/BSCB) in both patients and animal models. The present review provides an updated analysis of the microvascular pathology and impaired BBB/BSCB in ALS. Based on experimental and clinical ALS studies, the roles of cellular components, cell interactions, tight junctions, transport systems, cytokines, matrix metalloproteinases, and free radicals in the BBB/BSCB disruption are discussed. The impact of BBB/BSCB damage in ALS pathogenesis is a novel research topic, and this review will reveal some aspects of microvascular pathology involved in the disease and hopefully engender new therapeutic approaches.International Review of Neurobiology 01/2012; 102:91-106. DOI:10.1016/B978-0-12-386986-9.00004-1 · 2.46 Impact Factor
- The Journal of trauma 11/2011; 71(5):1480-1. DOI:10.1097/TA.0b013e3182331fd2 · 2.96 Impact Factor