サトウ キヨウコ   SATO Kyoko
  佐藤 恭子
   所属   医学部 医学科(東医療センター)
   職種   講師
論文種別 原著
言語種別 英語
査読の有無 査読あり
表題 Relationship between human evolution and neurally mediated syncope disclosed by the polymorphic sites of the adrenergic receptor gene α2B-AR.
掲載誌名 正式名:PloS one
略  称:PLoS One
ISSNコード:(1932-6203)1932-6203(Linking)
巻・号・頁 10(4),e0120788頁
著者・共著者 Komiyama Tomoyoshi, Hirokawa Takatsugu, Sato Kyoko, Oka Akira, Kamiguchi Hiroshi, Nagata Eiichiro, Sakura Hiroshi, Otsuka Kuniaki, Kobayashi Hiroyuki
発行年月 2015
概要 The objective of this study was to clarify the effects of disease on neurally mediated syncope (NMS) during an acute stress reaction. We analyzed the mechanism of the molecular interaction and the polymorphisms of the alpha-2 adrenoreceptor (α2B-AR) gene as the potential psychiatric cause of incentive stress. We focused on the following three genotypes of the repeat polymorphism site at Glu 301-303 in the α2B-AR gene: Glu12/12, Glu12/9, and Glu9/9. On the basis of our clinical research, NMS is likely to occur in people with the Glu12/9 heterotype. To verify this, we assessed this relationship with the interaction of Gi protein and adenylate cyclase by in silico analysis of the Glu12/9 heterotype. By measuring the difference in the dissociation time of the Gi-α subunit twice, we found that the Glu12/9 heterotype suppressed the action of adenylate cyclase longer than the Glu homotypes. As this difference in the Glu repeat number effect is thought to be one of the causes of NMS, we investigated the evolutionary significance of the Glu repeat number. Glu8 was originally repeated in simians, while the Glu12 repeats occurred over time during the evolution of bipedalism in humans. Taken with the Glu12 numbers, NMS would likely become a defensive measure to prevent significant blood flow to the human brain.
DOI 10.1371/journal.pone.0120788
PMID 25860977