Hironobu Katsuyama
   Department     ,
   Position  
Article types 原著
Language English
Peer review Peer reviewed
Title 17beta-estradiol inhibits chondrogenesis in the skull development of zebrafish embryos.
Journal Formal name:Aquatic toxicology (Amsterdam, Netherlands)
Abbreviation:Aquat Toxicol
ISSN code:0166445X
Volume, Issue, Page 95(4),292-298頁
Author and coauthor Fushimi Shigeko, Wada Naoyuki, Nohno Tsutomu, Tomita Masafumi, Saijoh Kiyofumi, Sunami Shigeo, Katsuyama Hironobu
Publication date 2009/12
Summary 17beta-Estradiol (E2) plays important roles in the development and differentiation of the gonad and central nervous systems, but little is known regarding the effects of exogenous E2 on chondrogenesis in skeletal development. In the present study, we found that treatment with E2 1–5 days post-fertilization (dpf) at concentrations above 1.5×10−5M increased the mortality rate in zebrafish embryos. Morphological analysis showed that treatment with E2 1–5 dpf caused abnormal cartilage formation in a dose-dependent manner at concentrations above 5×10−6 M. E2 1–5 dpf at 1.5×10−5Mcaused defects of the ethmoid plate, parallel cleft of the trabecular cartilage, and hypoplasia of Meckel’s cartilage and the ceratohyal cartilage. The sensitivity of embryos to E2 depended on the developmental stage. In early chondrogenesis (1–2 dpf), the embryoswere highly sensitive to E2, leading to hypoplasia of the cartilage. In situ hybridization studies showed that expression levels of patched1 (ptc1) and patched2 (ptc2) receptor mRNAs were markedly decreased by exposure to 2×10−5ME2 1–2 dpf.However, the expression levels of sonic hedgehog (shh) and tiggywinkle hedgehog (twhh) mRNAs were constant in the E2-treated embryos. In addition, the estrogen receptor antagonist ICI 182,780 did not completely abolish the effects of E2, suggesting that E2 may not inhibit chondrogenesis through its nuclear estrogen receptor. These results suggest that exposure to exogenous E2 possibly inhibits chondrogenesis via inhibition of the hedgehog (Hh) signal transduction system.
DOI 10.1016/j.aquatox.2009.03.004
Document No. 19386370