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• W2070832004 abstract "Abstract BACKGROUND: The current understanding of the effects of hypoxia on early embryogenesis is limited. Potential mediators of hypoxic effects include adenosine, which increases dramatically during hypoxic conditions and activates A 1 adenosine receptors (A 1 ARs). METHODS: To examine the influences of hypoxia and adenosine signaling on cardiac development, chicken embryos were studied. Real time RT‐PCR assay was used to examine the A 1 AR gene expression during embryogenesis and after siRNA‐ mediated knock down. Cell proliferation was determined by counting cell nuclei and PhosphoHistone H3 positive cells. Apoptosis was determined by TUNEL assay. RESULTS: A 1 ARs were found to be expressed in chicken embryos during early embryogenesis. Treatment of Hamburger and Hamilton stage 4 embryos with the A 1 AR agonist N 6 ‐cyclopentyladenosine caused cardiac bifida and looping defects in 55% of embryos. Hamburger and Hamilton stage 4 embryos exposed to 10% oxygen for 6, 12, 18, and 24 h followed by recovery in room air until stage 11, exhibited cardia bifida and looping defects in 34, 45, 60, and 86% of embryos respectively. Hypoxia‐induced abnormalities were reduced when A 1 AR signaling was inhibited by the A 1 AR antagonist 1,3 dipropyl‐8‐cyclopentylxanthine or by siRNA‐targeting A 1 ARs. Hypoxia treatment did not increase apoptosis, but decreased embryonic cell proliferation. CONCLUSIONS: These data indicate that hypoxia adversely influences cardiac malformations during development, in part by A 1 AR signaling. Birth Defects Research (Part A), 2008. © 2008 Wiley‐Liss, Inc." @default.
• W2070832004 created "2016-06-24" @default.
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• W2070832004 date "2008-01-09" @default.
• W2070832004 modified "2023-10-18" @default.
• W2070832004 title "Hypoxia induces cardiac malformations via A1 adenosine receptor activation in chicken embryos" @default.
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• W2070832004 doi "https://doi.org/10.1002/bdra.20438" @default.
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