Hsa_circ_0015382 is involved in the pathogenesis of preeclampsia by mediating THBS2 expression

Abstract

AbstractBackgroundPreeclampsia (PE) is a hypertensive disorder of pregnancy that causes significant maternal and perinatal morbidity and mortality. Circular RNA (circRNA) hsa_circ_0015382 is associated with the pathogenesis of PE, but its underlying regulatory mechanism remains to be explored.MethodsRelative RNA levels of hsa_circ_0015382, microRNA‐616‐3p and thrombospondin‐2 (THBS2) were detected by quantitative reverse transcription‐polymerase chain reaction. In vitro regulatory effects of hsa_circ_0015382 on the proliferation, migration, invasion and angiogenesis of trophoblasts were evaluated by CCK‐8, flow cytometry for cell cycle, EdU, transwell, wound healing and HUVEC tube formation assays, respectively. Targeting interaction was verified by dual‐luciferase reporter and RNA immunoprecipitation assays.ResultsHsa_circ_0015382 was highly expressed in placental tissues from PE patients. Upregulation of hsa_circ_0015382 repressed trophoblast proliferation, migration, invasion and lowered trophoblast‐induced HUVEC tube formation. Hsa_circ_0015382 was validated as a miR‐616‐3p sponge and miR‐616‐3p targeted THBS2. Hsa_circ_0015382 could mediate trophoblast proliferation, migration, invasion and regulate trophoblast‐induced HUVEC tube formation by sponging miR‐616‐3p and regulating THBS2 expression.ConclusionHsa_circ_0015382 is associated with the pathogenesis of PPE by regulating the miR‐616‐3p/THBS2 axis.Highlights Hsa_circ_0015382 is overexpressed in preeclampsia patients. Hsa_circ_0015382 inhibits trophoblast proliferation, migration, invasion and decreases trophoblast‐induced HUVEC tube formation. Hsa_circ_0015382 interacts with miR‐616‐3p to regulate THBS2 expression.