オオニシ ジュンジ  onishi junji
大西 淳之

  • 所属   東京家政大学  家政学部 栄養学科
  •     東京家政大学大学院  人間生活学総合研究科 健康栄養学専攻
  •     東京家政大学大学院  人間生活学総合研究科 人間生活学専攻
  •     東京家政大学短期大学部  短期大学部 栄養科
  • 職種   教授
論文種別 原著
言語種別 英語
査読の有無 査読あり
表題 Differential roles of rennin and angiotensinogen in the feto-maternal interface to the development of complications of pregnancy.
掲載誌名 正式名:Molecular Endocrinology
略  称:Mol.Endocrinol.
ISSNコード:08888809
掲載区分国外
巻・号・頁 19(5),pp.1361-1372
著者・共著者 ◎Takimoto-Ohnishi E1, Saito T, Ishida J, Ohnishi J, Sugiyama F, Yagami K, Fukamizu A.
発行年月 2005/02
概要 We previously identified a transgenic mouse model that developed pregnancy-associated hypertension (PAH) and intrauterine growth restriction (IUGR) by mating females expressing human angiotensinogen (hANG) with males expressing human renin (hRN). These phenotypic defects were not observed in the opposite type of mating combination, despite the feto-placental overexpression of hRN and hANG detected in both types of crossbreeding. Detailed analysis of transgene localization in the labyrinth and its permeability to the maternal circulation revealed that hRN produced in trophoblast giant cells was secreted into the maternal circulation, whereas hANG, produced in chorionic trophoblasts and trophoblastic epithelium, was undetectable in the maternal plasma, probably due to their distinct spatial and temporal expression in labyrinth. These results demonstrated that PAH and IUGR could be mediated by feto-placental hRN through its permeability to the maternal circulation, not by feto-placental hANG production. Furthermore, overexpression of maternally derived hANG in decidua and spiral arteries of pregnant females with PAH and IUGR raises the possibility of local activation of the renin-angiotensin system and its pathophysiological effects on placental hypoperfusion in complications of pregnancy. This study provides in vivo evidence that the cell-specific expression of RN and ANG in the feto-maternal interface impacts their differential roles in pregnancy.
DOI http://dx.doi.org/10.1210/me.2004-0158