イシイ　ヤスオ   石井　泰雄    所属   統合教育学修センター 統合教育学修センター    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	Induction of proepicardial marker gene expression by the liver bud.
掲載誌名	正式名：Development (Cambridge, England) 略　 称：Development ISSNコード：(0950-1991)0950-1991(Linking)
掲載区分	国外
巻・号・頁	134(20),pp.3627-37
著者・共著者	Ishii Yasuo, Langberg Jonathan D, Hurtado Romulo, Lee Sharrell, Mikawa Takashi
発行年月	2007/10
概要	Cells of the coronary vessels arise from a unique extracardiac mesothelial cell population, the proepicardium, which develops posterior to the sinoatrial region of the looping-stage heart. Although contribution of the proepicardial cells to cardiac development has been studied extensively, it remains unresolved how the proepicardium is induced and specified in the mesoderm during embryogenesis. It is known, however, that the proepicardium develops from the mesothelium that overlays the liver bud. Here, we show that the expression of proepicardial marker genes - Wt1, capsulin (epicardin, pod1, Tcf21) and Tbx18, can be induced in naïve mesothelial cells by the liver bud, both in vitro and in vivo. Lateral embryonic explants, when co-cultured with the liver bud, were induced to express these proepicardial marker genes. The same induction of the marker genes was detected in vivo when a quail liver bud was implanted in the posterior-lateral regions of a chick embryo. This ectopic induction of marker gene expression was not evident when other endodermal tissues, such as the lung bud or stomach, were implanted. This inductive response to the liver bud was not detectable in host embryos before stage 12 (16-somite stage). These results suggest that, after a specific developmental stage, a large area of the mesothelium becomes competent to express proepicardial marker genes in response to localized liver-derived signal(s). The developmentally regulated competency of mesothelium and a localized inductive signal might play a role in restricting the induction of the proepicardial marker gene expression to a specific region of the mesothelium. The data might also provide a foundation for future engineering of a coronary vascular progenitor population.
DOI	10.1242/dev.005280
PMID	17855432