Aberrant expression of solute carrier family transporters in placentas associated with pregnancy complications.

INTRODUCTION

Solute carrier family transporters (SLCs), crucial for nutrient and trace element uptake in the placenta, play a significant role in fetal growth and development. Their dysregulation is associated with various pregnancy disorders. However, a comprehensive understanding of their role and regulation in placental function and pregnancy complications is still a largely unexplored area, making this study novel and significant.

METHODS

We performed a rigorous meta-analysis of publicly available NCBI GEO microarray and RNA-Seq datasets followed by bioinformatics analysis of differentially expressed SLCs in PE and IUGR. The identified SLCs were then validated using qPCR on PE placental samples, ensuring the reliability and validity of the findings.

RESULTS

Bioinformatics analysis of preeclampsia (PE) and Intrauterine Growth restriction (IUGR) datasets revealed significant associations between specific SLC transporters with disease pathology, identified by studying differentially expressed SLCs. Subsequent validation using qPCR on placental samples confirmed considerable downregulation of SLC6A8, SLC16A10, SLC25A3, and SLC29A3, highlighting their dysregulation in the pathogenesis of PE and IUGR.

DISCUSSION: The significant downregulation of SLC6A8, SLC16A10, SLC25A3, and SLC29A3 observed by bioinformatics analyses and validated by qPCR indicates atypical expression of these SLCs in gestational disorders. Our findings underscore the potential contribution of multiple SLC gene families to the development of placental pathologies associated with diverse pregnancy complications.