Decorin inhibits the migration and invasion of the LPS + high glucose–induced primary trophoblast cell through ADAMTS12

Abstract Decorin was identified as the most relevant biomarker in type 2 diabetes or obesity-related diseases, but its function in gestational obesity or gestational diabetes mellitus (GDM) remains unknown. RT-qPCR or western blot were employed to validate the expression of Decorin and ADAMTS12 in the umbilical cord blood or placental tissues of the aforementioned groups. Subsequently, an LPS + high glucose–induced primary trophoblast cell model was established to verify the expression of DCN and ADAMTS12 in trophoblasts. Based on this model, silencing (si) of Decorin, or Decorin recombinant protein (DCN-r) combined with si-ADAMTS12 intervention, was performed to investigate its effects on trophoblast cell proliferation, migration, invasion, and other characteristics. Compared to the normal pregnancy group, the levels of DCN and ADAMTS12 showed an increasing trend in the gestational obesity group and the GDM group. Notably, DCN and ADAMTS12 were markedly higher in the GDM with obesity group compared to either the gestational obesity or GDM-alone groups. LPS + high glucose inhibited the migration and invasion of primary trophoblast cells while promoting increased levels of DCN and ADAMTS12. Under LPS + high-glucose intervention, DCN-r further suppressed trophoblast cell migration and invasion while enhancing ADAMTS12 expression, whereas si-DCN reversed these effects. Additionally, si-ADAMTS12 attenuated the LPS + high glucose–induced decline in trophoblast cell migration and invasion and blocked the promoting effects of DCN recombinant protein. Silencing ADAMTS12 can inhibit the promotive effect of DCN on the migration and invasion capabilities of LPS + high glucose–induced primary trophoblast cells. Clinical trial number: not applicable.