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Retinoic acid controls vascular formation by activating transcription of aryl hydrocarbon receptor gene in medakafish Oryzias latipes

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Retinoic acid controls vascular formation by activating transcription of aryl hydrocarbon receptor gene in medakafish Oryzias latipes

Material type
文書・図像類
Author
Sada, Naotakaほか
Publisher
-
Publication date
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Material Format
Digital
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type:textRetinoic acid (RA) has been shown to have a role in vascular formation, but how it affects is not fully understood. Previously, we reported t...

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  • Hiroshima University Institutional Repository

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Digital

Material Type
文書・図像類
Title
Retinoic acid controls vascular formation by activating transcription of aryl hydrocarbon receptor gene in medakafish Oryzias latipes
Author/Editor
Sada, Naotaka
Hanafusa, Takahiro
Onizuka, Yuichi
Hayashida, Yasufumi
Kageyama, Shota
Yamashita, Ichiro
Author Heading
Sada, Naotaka
Hanafusa, Takahiro
Onizuka, Yuichi
Hayashida, Yasufumi
Kageyama, Shota
Yamashita, Ichiro
Pages
1-26
Text Language Code
eng
Subject Heading
arly hydrocarbon receptor
common cardinal vein
retinoic acid
retinoic acid receptor
medakafish
Target Audience
一般
Note (General)
type:text
Retinoic acid (RA) has been shown to have a role in vascular formation, but how it affects is not fully understood. Previously, we reported that RA and its nuclear receptor (RAR) is required for transcription of ahr1 encoding an aryl hydrocarbon receptor (AHR), and that pharmacological modulation of RA, RAR, and AHR impairs the formation of common cardinal veins (CCVs) on the yolk of medakafish embryos. Here, to delineate a role for ahr1 in the vascular formation, we used an antisense-ahr1 mRNA to suppress ahr1. Following the development of vegfr1-expressing angioblast cells, we show that the antisense-ahr1 greatly inhibited the accumulation of angioblasts at the prospective branchial arch (PBA) where CCVs begin to develop on the yolk and the following CCV formation, demonstrating for the first time the essential role of ahr1 in the embryonic vascular formation of vertebrates. We also show that rarα and ahr1 mRNAs are co-expressed at PBA, suggesting a possible role of the specific expression.
This work was supported in part by a grant from the Ministry of Education, Science, Sports and Culture of Japan.
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