Poster Session K - Theoretical and Translational Medicine 2.
Introduction: Placental proteins play an important role during pregnancy processes, including trophoblast cell differentiation, maintenance of maternal-fetal immune tolerance and in the remodeling of maternal arteries. The dysregulation of placental proteins and the mechanisms they orchestrate can lead to pregnancy complications, such as preeclampsia and recurrent miscarriage. Among these proteins, placental galectins (gal-13, gal-14 - proteins of LGALS13, LGALS14) were found to be important components of the maternal-fetal interface as they influence maternal immune tolerance toward the developing fetus and their altered expression is linked to pregnancy complications.
Aims: To extend our knowledge, this study was aimed at uncovering the transcriptional and post-transcriptional regulation of LGALS13 and LGALS14 by bioinformatics analysis.
Methods: For the identification of relevant transcription factors and miRNAs targeting LGALS13 and LGALS14, prediction tools and high dimensional single cell data were used. Microarray and qRT-PCR data were used to intersect potential transcription factors with those which are differentially expressed in obstetrical syndromes.
Results: We identified several putative transcription factors that can regulate galectin expression. Fourteen were found to be downregulated in preeclampsia and recurrent pregnancy loss. miRNAs for LGALS13 and for LGALS14 were predicted by all the applied platforms, from which two were identical. According to our search, four miRNAs were already found in obstetrical syndromes to be upregulated, which could contribute to the downregulation of placental galectins in these pathological pregnancies.
Conclusion: Overall, this research enhances our understanding of the transcriptional and post-transcriptional regulation of placental proteins (focusing on placental galectins) and their potential role in pregnancy complications. However, further in vitro experiments are needed to validate these findings and to reveal their impact on maternal-fetal immunotolerance.
Funding: This research was funded by the MTA (LP2014-7/2014, Premium_2019-436) and by NKFIH (OTKA K128262, 2019-2.1.7-ERA-NET-2020-00014) grants. Supported by the ÚNKP-23-3 New National Excellence Program of the Ministry for Culture and Innovation from the source of the National Research, Development, and Innovation Fund (ÚNKP-23-3-II-ELTE-174).