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- 저자 : ( Yasuo Miki ) (검색결과 2 건)
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Genetics and Biomarkers of Moyamoya Disease: Significance of RNF213 as a Susceptibility Gene
Miki Fujimura,Shinya Sonobe,Yasuo Nishijima,Kuniyasu Niizuma,Hiroyuki Sakata,Shigeo Kure,Teiji Tominaga 대한뇌졸중학회 2014 Journal of stroke Vol.16 No.2
Moyamoya disease is characterized by a progressive stenosis at the terminal portion of the internal carotid artery and an abnormal vascular network at the base of the brain. Although its etiology is still unknown, recent genome-wide and locus-specific association studies identified RNF213 as an important susceptibility gene of moyamoya disease among East Asian population. A polymorphism in c.14576G>A in RNF213 was identified in 95% of familial patients with moyamoya disease and 79% of sporadic cases, and patients having this polymorphism were found to have significantly earlier disease onset and a more severe form of moyamoya disease, such as the presentation of cerebral infarction and posterior cerebral artery stenosis. The exact mechanism by which the RNF213 abnormality relates to moyamoya disease remains unknown, while recent reports using genetically engineered mice lacking RNF213 by homologous recombination provide new insight for the pathogenesis of this rare entity. Regarding biomarkers of moyamoya disease, moyamoya disease is characterized by an increased expression of angiogenic factors and pro-inflammatory molecules such as vascular endothelial growth factors and matrix metalloproteinase-9, which may partly explain its clinical manifestations of the pathologic angiogenesis, spontaneous hemorrhage, and higher incidence of cerebral hyperperfusion after revascularization surgery. More recently, blockade of these pro-inflammatory molecules during perioperative period is attempted to reduce the potential risk of surgical complication including cerebral hyperperfusion syndrome. In this review article, we focus on the genetics and biomarkers of moyamoya disease, and sought to discuss their clinical implication.
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( Yukie Kidani ),( Yasuo Miki ),( Nana Nomimura ),( Shiori Minakawa ),( Norifumi Tanaka ),( Hiroshi Miyoshi ),( Koichi Wakabayashi ),( Yoshiki Kudo ) 대한산부인과학회 2016 대한산부인과학회 학술대회 Vol.102 No.-
Objectives: Hypoxic-ischemic encephalopathy (HIE) is a major cause of cerebral palsy in full-term infants. HIE occurs at a rate of about three per thousand live-born infants, even in developed countries. In recent years stem cell therapies have been applied in several fields of medicine. Endothelial progenitor cells (EPCs) are one of the major stem/progenitor cell subsets with the potential for repairing vascular injury. Therefore, we have speculated that the transplantation of CD133<sup>+</sup> cells, as a EPCs containing fraction, from umbilical cord blood could also be an useful therapy in perinatal hypoxia-induced brain injury. We established the ex vitro hypoxic-ischemic encephalopathy model to assess the effects of CD133<sup>+</sup> cells (endothelial progenitor cells) derived from human umbilical cord blood on nerve extension. In this study, we have investigated the therapeutic effects of CD133<sup>+</sup> cells for the treatment of neonatal HIE on an animal model. Methods: Hypoxic-ischemic brain lesions were induced in neonatal severe combined immunodeficiency mice using the Rice-Vanucci method. CD133<sup>+</sup> cells were administered by intraperitoneal injection 24 h after injury. Macroscopic assessment, growth evaluation and immunohistochemical analysis were performed. To evaluate motor function, rotarod test was performed every 7days between day 28 and day 56 of postnatal. Results: Immunohistochemical analysis revealed that intraperitoneally transplanted CD133<sup>+</sup> cells migrate towards the brain 48 h after injection. The ratio of lesioned to non-lesioned hemisphere area in the CD133<sup>+</sup> group was significantly higher than in the HI group. Moreover, in CD133<sup>+</sup> cell-treated animals, motor function improved and the brain was protected from the hypoxic-ischemic insult compared with untreated animals. Conclusion: Our results suggest that CD133<sup>+</sup> cells derived from human umbilical cord blood have therapeutic po-tential in neonatal hypoxic-ischemic encephalopathy.
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