Epigenetic status of imprinted genes in placenta during recurrent pregnancy loss

Саженова, Е. А.; Nikitina, Tatiana; Skryabin, N. A.; Minaycheva, L. I.; Ivanova, Tatyana V.; Nemtseva, T. N.; Yuriev, S. Yu.; Евтушенко, И. Д.; Lebedev, I. N.

doi:10.1134/s1022795417020090

Cited by 10 publications

(1 citation statement)

References 29 publications

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“…Furthermore, we can not ignore that the controls used, although corresponding to pregnancy losses with a non-genetic cause (infections), do not represent normal pregnancies (without any kind of complications). We may also point out that only a few imprinted genes have been studied and that we may be faced with a complex and coordinated network of imprinted genes responsible for intrauterine development [45]. To acquire a better knowledge about the etiology of the loss of human pregnancy more studies on the molecular mechanism underlying the expression of imprinted genes are needed.…”

Section: Discussionmentioning

confidence: 99%

Altered expression of epigenetic regulators and imprinted genes in human placenta and fetal tissues from second trimester spontaneous pregnancy losses

et al. 2019

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Epigenetic mechanisms such as genomic imprinting have a fundamental role in embryo and fetal development. Hence, we here studied expression levels of epigenetic modifiers and imprinted genes in cases of ididopathic spontaneous abortion (SA). Thirty-five placental samples and 35 matched fetal tissues from second trimester SA were analysed; including 16 controls (placental and fetal infections as the known cause of spontaneous abortion) and 19 idiopathic SA cases. Transcript levels of epigenetic regulators and imprinted genes were measured by qRT-PCR and methylation at imprinted genes was studied by bisulfite genomic sequencing and MS-MLPA. Global DNA hydroxymethylation (5-hmC) levels were measured by an ELISA-based assay. We observed an upregulation of TET2 and TET3 in placental samples from idiopathic SA cases; however, no significant difference in global 5-hmC levels was observed. On the contrary, in fetal tissues, TET3 was markedly downregulated in idiopathic SA, showing an opposite trend to that observed in placental tissue. IGF2 and CDKN1C were upregulated and MEST downregulated in placentas from idiopathic SA cases; concordantly, IGF2 was also upregulated in fetal tissues from idiopathic SA cases. Although not reaching statistical significance, an increase in methylation levels of MEST, KvDMR1 and H19 DMRs was observed in idiopathic SA cases, concordantly with the observed changes in expression. Our study reveals, for the first time, deregulation of epigenetic modifiers and imprinted genes in both placental and fetal tissues from idiopathic SA cases in the second trimester of pregnancy, indicating a critical role during pregnancy.

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Section: Discussionmentioning

confidence: 99%