2013
DOI: 10.1016/j.mce.2013.08.011
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Heparin-binding epidermal growth factor-like growth factor (HB-EGF) induction on Snail expression during mouse decidualization

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Cited by 17 publications
(17 citation statements)
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“…4) or Rev-erb␣-siRNA (data not shown). Therefore, during decidualization, it is considered that Ptgs2 induction requires the intracellular downregulation of Rev-erb␣ as well as the extracellular inducible signals previously reported, such as those by cytokines, ovarian steroid hormones, growth factors, and PGs (11,28,29,58). In Fig.…”
Section: Discussionmentioning
confidence: 93%
“…4) or Rev-erb␣-siRNA (data not shown). Therefore, during decidualization, it is considered that Ptgs2 induction requires the intracellular downregulation of Rev-erb␣ as well as the extracellular inducible signals previously reported, such as those by cytokines, ovarian steroid hormones, growth factors, and PGs (11,28,29,58). In Fig.…”
Section: Discussionmentioning
confidence: 93%
“…PR could be involved in regulating Snail, a transcription repressor which has recently been identified to play a central role in the epithelial-mesenchymal transition in which its expression has been reported to be induced by HB-EGF via EGFR-ERK-STAT3 signaling pathway [99]. HOXA-10, an abdominal-like homeobox gene reported to be involved in the decidualization process, could also be influenced by PR where loss of Hoxa-10 function in mice has been reported to result in infertility [100].…”
Section: Role Of Pgs In Decidualizationmentioning
confidence: 99%
“…Human trophoblast differentiation is regulated by redox balance because early trophoblast differentiation or invasion alterations lead to pregnancy complications such as an abnormal placentation. Snail expression is sensitive to hypoxia, either directly through activation of the HIF-1α responsive element on its promoter or by epidermal growth factor (EGF), transforming growth factor (TGF), α, β, and tumoral necrosis factor (TNFα) mediators activated by hypoxic signals [2][3][4]. Snail upregulation by HIF-1α in cultured human first trimester villous explants reduces E-cadherin expression and activates an invasion program [5].…”
Section: Introductionmentioning
confidence: 99%