Publications (3)6.73 Total impact
Article: Dynamic changes of vascular endothelial growth factor and angiopoietin-1 in association with circulating endothelial progenitor cells after severe traumatic brain injury.[show abstract] [hide abstract]
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.The Journal of trauma 06/2011; 70(6):1480-4. · 2.48 Impact Factor
Article: Correlation of CD34+ cells with tissue angiogenesis after traumatic brain injury in a rat model.[show abstract] [hide abstract]
ABSTRACT: Increasing evidence suggests that circulating endothelial progenitor cells, which are a subpopulation of hematopoietic progenitor CD34(+) cells, play a critical role in neovascularization and tissue repair. We have tested the hypothesis that traumatic brain injury (TBI) could mobilize CD34(+) cells to peripheral blood and brain tissue, a process critical for vascular repair, in a rat model of TBI. Male Wistar rats were subjected to controlled fluid percussion. Blood and brain tissue were collected before and after TBI to measure the levels of CD34(+) cells in peripheral blood and to detect their accumulation in the damaged cerebral tissue. Compared with surgery controls, CD34(+) cells significantly increased in the peripheral blood and accumulated in the brain tissue of TBI rats. Immunohistochemistry detected new vessels with incomplete CD34(+) endothelial-like cell lining and an increased number of microvessels in the injured and surrounding tissue. The results demonstrate a close correlation between an increase in circulating CD34(+) cells in response to traumatic injury and angiogenesis in TBI rat brain. They also suggest that transplantation of CD34(+) cells or augmentation of endogenous CD34(+) cells may be a novel therapeutic approach for patients with TBI.Journal of neurotrauma 03/2009; 26(8):1337-44. · 4.25 Impact Factor
Article: Amelioration of β654-thalassemia in mouse model with the knockdown of aberrantly spliced β-globin mRNA[show abstract] [hide abstract]
ABSTRACT: Large amounts of aberrantly spliced mRNA from the β654 allele was present in erythroid cells, which might impair the erythropoiesis. A therapeutic strategy for β-thalassemia was explored by knocking down the aberrantly spliced mRNA of β-globin. Lentiviral vector with siRNA fragment targets on the specific portion of β654-globin aberrantly spliced pre-mRNA was constructed. In HeLa β654 cells, the siRNA vector could reduce approximately 60% of aberrantly spliced mRNA, which was assessed by RT-PCR and qRT-PCR. Furthermore, a disease model of β654 thalassemia mice with lentiviral-mediated siRNA was produced by subzonal injection (named Hβi-Hbbth-4/Hbb+ transgenic mice). Our results showed that the hemotological parameters were improved in Hβi-Hbbth-4/Hbb+ transgenic mice. This study provides a potential way for β654-thalassemia therapy by knocking down the aberrantly spliced β-globin mRNA, whilst supporting that the aberrantly spliced β-globin mRNA may aggravate the disease.Journal of Genetics and Genomics.