The following is a summary of “Blocking the interaction between circTNRC18 and LIN28A promotes trophoblast epithelial-mesenchymal transformation and alleviates preeclampsia,” published in the January 2024 issue of Endocrinology by Chen, et al.
The condition known as preeclampsia (PE) is characterized by abnormalities in migration and invasion brought on by dysregulation of trophoblastic epithelial–mesenchymal transition (EMT). They have shown in the past that circTNRC18 is capable of inhibiting the migration and EMT of trophoblasts; however, the function that it plays in PE is still unclear. For a study, researchers sought to show that circTNRC18 interacts with lin-28 homolog, a (LIN28A), an RNA-binding protein, and that this connection is augmented in placental tissue from a patient with peritoneal fibrosis.
The suppression of trophoblast migration, invasion, and EMT mediated by circTNRC18 is suppressed by LIN28A overexpression, while the promotion of these processes is facilitated by LIN28A knockdown. circTNRC18 is responsible for regulating the intracellular distribution of LIN28A. Within the cell, it stabilizes the mRNA of insulin-like growth factor II, which stimulates the production of insulin-like growth factor II. By blocking the interaction between LIN28A and GATA1, circTNRC18 also facilitates the development of complexes between GATA-binding factor 1 (GATA1) and sine oculis homeobox 1 (SIX1).
The transcription of grainy head-like protein 2 homologs and the control of cell migration and invasion by circTNRC18 are both driven by GATA1–SIX1, which enhances their expression. Furthermore, in a model with lower uterine perfusion pressure, PE may be alleviated by inhibiting the interaction between circTNRC18 and LIN28A using antisense nucleotides. Therefore, addressing the regulatory axis connected to circTNRC18 and LIN28A might be an innovative approach to treating PE.
Source: sciencedirect.com/science/article/abs/pii/S0303720723002241
