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Hypoxia induces microRNA miR-210 in vitro and in vivo ephrin-A3 and neuronal pentraxin 1 are potentially regulated by miR-210.

Abstract
Shortage of oxygen is one of the prime stress conditions in tissues. In this study, we looked for microRNAs expressed during hypoxia and showed that miR-210 expression was upregulated in response to hypoxia in vitro and in vivo. An active form of the HIF-1alpha induced the expression of miR-210, showing the involvement of the HIF-1 signaling pathway in miR-210 gene transcription. Furthermore, miR-210 was shown to bind to the predicted target sites of ephrin-A3 or neuronal pentraxin 1, causing repression in luciferase reporter activity. Contrary to the microRNA-mediated repression hypothesis, ephrin-A3 was expressed at very high levels in post-ischemic mouse hippocampus in vivo. Thus, the regulatory effects of miR-210 on its targets in vivo need to be further characterized.
AuthorsKati Pulkkinen, Tarja Malm, Mikko Turunen, Jari Koistinaho, Seppo Ylä-Herttuala
JournalFEBS letters (FEBS Lett) Vol. 582 Issue 16 Pg. 2397-401 (Jul 09 2008) ISSN: 0014-5793 [Print] England
PMID18539147 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • 3' Untranslated Regions
  • Ephrin-A3
  • MicroRNAs
  • Nerve Tissue Proteins
  • RNA, Messenger
  • neuronal pentraxin
  • C-Reactive Protein
Topics
  • 3' Untranslated Regions (chemistry)
  • Animals
  • Brain Ischemia (metabolism)
  • C-Reactive Protein (genetics, metabolism)
  • Cell Hypoxia
  • Cell Line, Tumor
  • Cells, Cultured
  • Ephrin-A3 (genetics, metabolism)
  • Gene Expression Regulation
  • Humans
  • Mice
  • MicroRNAs (biosynthesis, chemistry, metabolism)
  • Nerve Tissue Proteins (genetics, metabolism)
  • RNA, Messenger (metabolism)
  • Rabbits

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