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Fengming Lan, Qing Qin, Huiming Yu and Xiao Yue

negative controls (miR-NC) purchased from GenePharma. HIF-1α full-length genomic DNA was amplified and cloned into a pcDNA3 vector to construct the HIF-1α vector. Lipofectamine 2000 reagent (Invitrogen) was used to transfect all synthetic compounds. Patients and Clinical Samples This study was approved by Tianjin Huanhu Hospital, Beijing Sanbo Brain Hospital, Beijing University Cancer Hospital, and Tianjin Hospital. All participants signed appropriate informed consent for collection of blood and tumor tissue samples prior to study recruitment. Eighty patients with

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David L. Gillespie, Maria T. Aguirre, Sandhya Ravichandran, Lisa L. Leishman, Claudia Berrondo, Joseph T. Gamboa, Libo Wang, Rose King, Xuli Wang, Mingqian Tan, Anthony Malamas, Zheng-Rong Lu and Randy L. Jensen

transcription factor hypoxia-inducible factor 1α (HIF-1α), and other hypoxia-regulated proteins, such as VEGF, carbonic anhydrase-IX (CA-IX), the receptor tyrosine kinase c-MET, and glucose transporter 1 (GLUT-1), 5 , 26 , 29 are overexpressed in malignant brain tumors. 54 , 66 HIF-1α protein levels, tumor grade, and vascularity have been correlated in brain tumors, 14 , 66 and studies have shown that hypoxia markers are predictive of outcomes for patients with a number of tumor types. 17 , 22 , 37 The transcription factor HIF-1 is composed of 2 heterodimeric subunits

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Xiang Zou, Liangfu Zhou, Wei Zhu, Ying Mao and Liang Chen

analysis and real-time polymerase chain reaction (RT-PCR) analysis. All 6 rats in each group were used for plasma enzyme-linked immunosorbent assay examination. Immunohistochemistry Dural tissue samples were fixed in 10% formalin, embedded in paraffin, sectioned at 4-μm thicknesses, and stained with anti-CD31 (rabbit monoclonal antibody [Abcam, HK Ltd.]), inhibitor of differentiation 1 (ID-1), hypoxia-inducible factor 1α (HIF-1α), vascular endothelial growth factor (VEGF), and matrix metalloproteinases 2 and/or 9 (MMP-2/9) antibodies (rabbit polyclonal antibodies

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Randy L. Jensen, Scott Soleau, Mihir K. Bhayani and Dustin Christiansen

M eningiomas are the most common benign brain tumors in humans. 23, 25 Elevated VEGF expression has been demonstrated in meningiomas, 2, 43 and is associated with recurrence, 50 neovascularization, 35, 39 peritumoral edema, 3, 10, 18, 35, 51 and classifications of atypical or malignant according to the WHO scale. 21 Although these correlations have been disputed, 7, 34 the evidence indicates that VEGF plays an important role in meningioma tumorigenesis and growth. Transcription of VEGF is usually regulated by the transcription factor HIF-1α under

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Tetsuhiro Higashida, Christian W. Kreipke, José A. Rafols, Changya Peng, Steven Schafer, Patrick Schafer, Jamie Y. Ding, David Dornbos III, Xiaohua Li, Murali Guthikonda, Noreen F. Rossi and Yuchuan Ding

The role of MMPs in BBB disruption is further supported by the observation that treatment with MMP inhibitors decreases such disruption and improves brain edema. Similar to the case of AQP-4, however, the molecular cascade leading to the upregulation of MMP-9 after TBI is not clearly understood. 14 , 19 , 35 , 36 Hypoxia-inducible factor-1α (HIF-1α), an upstream transcription factor induced by hypoxia, regulates the subsequent expression of many kinds of proteins responding to the various pathophysiological conditions induced by hypoxia. 30 While some studies

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Hua-Jun Zhou, Tao Tang, Han-Jin Cui, A-Li Yang, Jie-Kun Luo, Yuan Lin, Qi-Dong Yang and Xing-Qun Li

factors, such as HIF-1α, VEGF, and Ang-2. 28 However, evidence has revealed that the reduction of cerebral blood flow adjacent to a hematoma is temporary and mild. 40 Therefore, we speculate that there may be factors other than hypoxia that trigger ICH-related angiogenesis. Thrombin, a serine protease activated from prothrombin, is released during hematoma formation after ICH. Thrombin has been proved to play a key role in ICH-induced brain damage. High concentrations of thrombin cause brain edema and cell death, while low concentrations are neuroprotective. 15 , 38

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Randy L. Jensen, David Gillespie, Paul House, Lester Layfield and Clough Shelton

regulation of HIF-1α. 10, 36, 39 Constitutive expression of HIF-1α has been detected in the cancer cells related to VHL disease. 49, 63, 67, 87 During conditions of low O 2 tension (1–2% O 2 ), degradation of HIF-1α is inhibited by O 2 -dependent hydroxylation of the protein that prevents interaction of HIF-1α with pVHL ubiquitin ligase complex ( Fig. 1 ). 4, 36, 39, 50, 70 The HIF-1α then binds to a DNA sequence known as HREs, and induces the transcription of a number of well-characterized genes that help cells “cope” with low O 2 conditions; these include VEGF and

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Tetsuhiro Higashida, Hiroshi Kanno, Masato Nakano, Kengo Funakoshi and Isao Yamamoto

. Several studies of human CA plaque have shown that many angiogenic proteins and apoptosis-inducible proteins are involved in plaque progression and instability. 32 , 34 However, there has been no study that shows the simultaneous expression of HIF-1α, VEGF, and Ets-1 except in a rat artery model. 20 We hypothesized that the hypoxia-induced HIF-1α/VEGF/Ets-1 cascade was also important for angiogenesis in human atherosclerosis. Therefore, the purpose of this study was to investigate whether these hypoxia-inducible angiogenic proteins play a major role in angiogenesis

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Eric M. Thompson, Nathaniel L. Whitney, Y. Jeffrey Wu and Edward A. Neuwelt

H ypoxia is a key component of aggressive behavior in many types of neoplasms. Hypoxia upregulates the transcription factor HIF-1α, which regulates signaling pathways involved in glycolysis, growth-factor signaling, tissue invasion, proliferation, 9 and expression of VEGF in angiogenesis. 27 Hypoxic conditions increase glioma cell migration, 2 and increasing HIF-1α expression correlates with increasing glioma grade, 18 particularly in the pseudopalisading cells in glioblastoma. 2 Hypoxia-inducible factor–1β is a constitutively expressed protein that

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Daina Kashiwazaki, Masaki Koh, Haruto Uchino, Naoki Akioka, Naoya Kuwayama, Kyo Noguchi and Satoshi Kuroda

that the expression of hypoxia-inducible factor-1 alpha (HIF-1α) and vascular endothelial growth factor (VEGF) is associated with IPH in carotid stenosis. 9 , 17 However, the detailed pathological mechanisms through which microvessels and IPH develop remain obscure. Endothelial progenitor cells (EPCs) are involved in neovascularization (CD31 positive) and endothelial integrity. There is growing evidence that some EPC subpopulations, characterized by surface markers such as CD34, VEGF receptor-2 (VEGFR-2), or CD133, might exert protective properties in