Abstract

Preterm birth is the leading cause of infant mortality. The mechanisms that instigate preterm birth remain elusive and this makes it difficult to predict or prevent preterm birth. In this study, we found that SP-A induced the pathological damage to placenta and promoted preterm birth. Mechanismly, SP-A promoted the expression of STOX1 which further promoted the oxidative stress in placenta through inhibiting the activities of series antioxidant enzymes including SOD, CAT1 and GSH-Px. SP-A also induced dysregulation of arginine metabolism through inhibiting NOS2 and ARG2. Overexpression of STOX1 aggravated SP-A induced oxidative stress, pathological damage and preterm birth, whereas knockdown of STOX1 alleviated SP-A induced oxidative stress, pathological damage and preterm birth. Our study uncovers that SP-A induces preterm birth through promoting oxidative stress via upregulating STOX1, which provides new targets for prediction and prevention of preterm birth.

Keywords: Antioxidant, Enzymes, Corticotropin-releasing hormone, Placental cells, Oxidative stress, Necrosis, Apoptosis