Data supporting 'Regulation of endometrial gland secretome sialylation and its implication in the pathogenesis of early-onset preeclampsia’

Dataset split into different chapter supporting the thesis.

  

Glycosylation is a post-translational modification that involves the enzymatic attachment of glycans to proteins or other organic molecules. Hormonal regulation of endometrial gland secretome glycosylation during the early placentation has suggested to be crucial for trophoblast functions and placental development. However, direct evidence for the involvement of protein glycosylation on regulating placentation is lacking. Previous studies had linked various pregnancy anomalies to the defects of glycosylation in placenta and uterus. Preeclampsia (PE) is one of these complications characterized by dysregulated invasion and migration of the trophoblast. Therefore, we hypothesize that the glycosylation of endometrial gland secretome is able to modulate trophoblast-regulatory activity of human and contributes to PE pathogenesis.

The human endometrial organoids (EO) were derived from endometrial tissues of patients who underwent In vitro fertilisation (IVF) in LH +7/8 stage. EOs were treated with sex hormones estrogen (E2), progesterone (P4), and human chorionic gonadotropin (hCG) to mimic the menstrual cycle and early pregnancy environment. The PE and normotensive (NT) EO culture were also established from the decidual tissues of women diagnosed with PE or not during their cesarean delivery. The organoid secretomes were collected for glycosylation profile by lectin array, lectin binding assay and sialo-proteomics analysis. Their roles on trophoblast functions e.g. differentiation, invasion and migration were also studied.

We have cultured EOs in hormonal conditions mimicking the proliferative phase (E2), secretory phase (E2+P4) and early pregnancy state (E2+P4+hCG). 

The project demonstrated that changes in the sialylation of endometrial gland secretome is associated with the alterations in trophoblast functions, which further indicated the importance of secretome glycoprotein sialylation in the PE pathophysiology.