机构：[1]Center for Cerebrovascular Research, Department of Anesthesia and Perioperative Care, University of California,San Francisco, CA[2]Department of Neurological Surgery, University of California, San Francisco, CA[3]Department of Neurology, University of California, San Francisco, CA[4]Department of Neurosurgery, Xuanwu Hospital, Capital University of Medical Sciences, Beijing, China神经外科首都医科大学宣武医院[5]Med-X Research Institute, Shanghai JiaoTong University, Shanghai, China[6]Department of Neurosurgery, Tongji Hospital, Tongji University, Shanghai, China
Cerebral venous hypertension (VH) and angiogenesis are implicated in the pathogenesis of brain arteriovenous malformation and dural arteriovenous fistulae. We studied the association of VH and angiogenesis using a mouse brain VH model. Sixty mice underwent external jugular vein and common carotid artery (CCA) anastomosis (VH model), CCA ligation, or sham dissection (n = 20). Hypoxia-inducible factor-1 alpha (HIF-1 alpha), vascular endothelial growth factor (VEGF) and stromal-cell-derived factor-1 alpha (SDF-1 alpha) expression, and matrix metalloproteinase (MMP) activity were analyzed. We found VH animals had higher (P < 0.05) sagittal sinus pressure (8 +/- 1 mmHg) than control groups (1 +/- 1 mmHg). Surface cerebral blood flow and mean arterial pressure did not change. Hypoxia-inducible factor-1 alpha, VEGF, and SDF-1 alpha expression increased (P < 0.05). Neutrophils and MMP-9 activity increased 10-fold 1 day after surgery, gradually decreased afterward, and returned to baseline 2 weeks after surgery. Macrophages began to increase 3 days after surgery (P < 0.05), which coincided with the changes in SDF-1 alpha expression. Capillary density in the parasagittal cortex increased 17% compared with the controls. Our findings suggest that mild nonischemic VH results in a pro-angiogenic stage in the brain by upregulating HIF-1 and its downstream targets, VEGF and SDF-1 alpha, increasing leukocyte infiltration and MMP-9 activity. Journal of Cerebral Blood Flow & Metabolism (2009) 29, 1482-1490; doi: 10.1038/jcbfm.2009.67; published online 27 May 2009
基金：
the National Institutes of Health (NS27713 and NS044155 to WLY), and the American Heart Association (SDG 0535018N to HS).
第一作者机构：[1]Center for Cerebrovascular Research, Department of Anesthesia and Perioperative Care, University of California,San Francisco, CA[4]Department of Neurosurgery, Xuanwu Hospital, Capital University of Medical Sciences, Beijing, China[6]Department of Neurosurgery, Tongji Hospital, Tongji University, Shanghai, China
通讯作者：
通讯机构：[*]University of California, San Francisco Department of Anesthesia and Perioperative Care 1001 Potrero Ave, Room 3C-38 San Francisco, CA 94110
推荐引用方式(GB/T 7714)：
Peng Gao,Yiqian Zhu,Feng Ling,et al.Nonischemic cerebral venous hypertension promotes a pro-angiogenic stage through HIF-1 downstream genes and leukocyte-derived MMP-9[J].JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM.2009,29(8):1482-1490.doi:10.1038/jcbfm.2009.67.
APA：
Peng Gao,Yiqian Zhu,Feng Ling,Fanxia Shen,Brian Lee...&William L. Young.(2009).Nonischemic cerebral venous hypertension promotes a pro-angiogenic stage through HIF-1 downstream genes and leukocyte-derived MMP-9.JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM,29,(8)
MLA：
Peng Gao,et al."Nonischemic cerebral venous hypertension promotes a pro-angiogenic stage through HIF-1 downstream genes and leukocyte-derived MMP-9".JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM 29..8(2009):1482-1490
医学