Background: The precise origin of Pre-eclampsia (PE) remains elusive. Multiple pieces of evidence support the existence of hypoxia in PE. MiRNA-210 (miR-210), which is induced by Hypoxia-Inducible Factor-1 alpha (HIF-1 alpha.) during hypoxia, is one of the most hypoxia sensitive miRNAs.MiR-210 mediates these functions by regulating a lot of target mRNAs. Protein tyrosine phosphatase, non-receptor type 2 (PTPN2) was one of miR-210 targets and was found to be down regulated by hypoxia. Objective: To assess the levels of relative expression of miR-210 and its target PTPN2 in Egyptian women with PE. This is in order to clarify their possible role in the progression of PE and their relation to each other and to different clinicopathological factors. Study design: Group1 included 35 normal primigravida and group 2 included 35 primigravida patients with PE. PE group was subdivided into-mild and severe (PE). Total RNA was extracted from placental tissue samples and Real-Time PCR was performed on the extracted RNA. Results: There was a highly significant difference between the studied groups as regards fold change of placental miR-210 and PTPN2 (P < 0.01). There was a highly significant negative correlation between miR-210 and PTPN2 RQ among the studied groups and among the preeclampsia group (P < 0.01). Conclusion: The results of this study demonstrated that placental expression of miR-210 was up regulated in pregnancies complicated with PE in comparison to normal pregnancies. This increase in miR-210 resulted in down regulation of its target PTPN2 mRNA and this can have a direct role in the pathogenesis of the PE disease. Additionally, both miR-210 & PTPN2 relative expression could differentiate between mild & severe PE. (C) 2016 Elsevier B.V. All rights reserved.
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Univ Paris Diderot, CNRS UMR 8251, Sorbonne Paris Cite, Unite Biol Fonct & Adaptat, F-75013 Paris, FranceUniv Paris Diderot, CNRS UMR 8251, Sorbonne Paris Cite, Unite Biol Fonct & Adaptat, F-75013 Paris, France
Bui, Linh-Chi
Berthelet, Jeremy
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Univ Paris Diderot, CNRS UMR 8251, Sorbonne Paris Cite, Unite Biol Fonct & Adaptat, F-75013 Paris, FranceUniv Paris Diderot, CNRS UMR 8251, Sorbonne Paris Cite, Unite Biol Fonct & Adaptat, F-75013 Paris, France
Berthelet, Jeremy
Dairou, Julien
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Univ Paris Diderot, CNRS UMR 8251, Sorbonne Paris Cite, Unite Biol Fonct & Adaptat, F-75013 Paris, FranceUniv Paris Diderot, CNRS UMR 8251, Sorbonne Paris Cite, Unite Biol Fonct & Adaptat, F-75013 Paris, France
Dairou, Julien
Mathieu, Cecile
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Univ Paris Diderot, CNRS UMR 8251, Sorbonne Paris Cite, Unite Biol Fonct & Adaptat, F-75013 Paris, FranceUniv Paris Diderot, CNRS UMR 8251, Sorbonne Paris Cite, Unite Biol Fonct & Adaptat, F-75013 Paris, France
Mathieu, Cecile
Guidez, Fabien
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Univ Paris Diderot, Inst Univ Hematol, Sorbonne Paris Cite, INSERM UMR S1131, F-75010 Paris, FranceUniv Paris Diderot, CNRS UMR 8251, Sorbonne Paris Cite, Unite Biol Fonct & Adaptat, F-75013 Paris, France
Guidez, Fabien
Dupret, Jean-Marie
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Univ Paris Diderot, CNRS UMR 8251, Sorbonne Paris Cite, Unite Biol Fonct & Adaptat, F-75013 Paris, FranceUniv Paris Diderot, CNRS UMR 8251, Sorbonne Paris Cite, Unite Biol Fonct & Adaptat, F-75013 Paris, France
Dupret, Jean-Marie
Cools, Jan
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VIB Ctr Biol Dis, Leuven, BelgiumUniv Paris Diderot, CNRS UMR 8251, Sorbonne Paris Cite, Unite Biol Fonct & Adaptat, F-75013 Paris, France
Cools, Jan
Chomienne, Christine
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Hop St Louis, AP HP, Serv Biol Cellulaire, F-75010 Paris, FranceUniv Paris Diderot, CNRS UMR 8251, Sorbonne Paris Cite, Unite Biol Fonct & Adaptat, F-75013 Paris, France
Chomienne, Christine
Rodrigues-Lima, Fernando
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Univ Paris Diderot, CNRS UMR 8251, Sorbonne Paris Cite, Unite Biol Fonct & Adaptat, F-75013 Paris, FranceUniv Paris Diderot, CNRS UMR 8251, Sorbonne Paris Cite, Unite Biol Fonct & Adaptat, F-75013 Paris, France