Suppression of circular RNA serum and glucocorticoid‐induced kinase 1 elevates antioxidant molecules and angiogenesis in trophoblast cells to attenuate preeclampsia via microRNA‐508‐3p to target and restrain PUM homolog 1

Abstract Aim Preeclampsia (PE) is a pregnancy‐specific syndrome characterized by hypertension and proteinuria. Recently, multiple circular RNAs (circRNAs) were considered latent clinical diagnostic markers or therapeutic targets. This study was to explore the impact of circRNA serum and glucocorticoid‐induced kinase 1 (SGK1) on PE via influencing the microRNA (miR)‐508‐3p/PUM homolog 1 (PUM1) axis. Methods Placental tissues of 34 pregnant women with PE and 34 normal pregnant women were collected to measure circRNA SGK1 (circSGK1), miR‐508‐3p, and PUM1. Human placental trophoblasts HTR‐8/SVneo were transfected with plasmids, thereafter to observe proliferation, migration, invasion, and apoptosis, analyze antioxidant molecules Troxerutin (TXN), Glutamate‐cysteine ligase catalytic subunit (GCLC), NAD (P) H‐quinone oxidoreductase 1 (NQO1), and determine angiogenesis. After the construction of the PE rat model, antioxidant molecules TXN, GCLC, and NQO1, vascular‐associated factor vascular endothelial growth factor A (VEGF‐A), and histopathological conditions were tested. Examination of the binding of circSGK1 and miR‐508‐3p with PUM1 was performed. Results Our data showed that circSGK1 expression was elevated in the placenta of patients with PE. Silenced circSGK1 or elevated miR‐508‐3p promoted the growth and antioxidant molecules and angiogenesis in trophoblast cells; CircSGK1 combined with miR‐508‐3p, and miR‐508‐3p targeted PUM1. Conclusions In summary, suppression of circSGK1 augments antioxidant molecules and angiogenesis in trophoblast cells to attenuate PE via miR‐508‐3p to target PUM1.