Spiral artery remodeling is an important physiological process in the pregnant uterus which increases blood flow to the fetus. Impaired spiral artery remodeling contributes to preeclampsia, a major disease in pregnancy. Corin, a transmembrane serine protease, is up-regulated in the pregnant uterus to promote spiral artery remodeling. To date, the mechanism underlying uterine corin up-regulation remains unknown. Here we show that Krüppel-like factor (KLF) 17 is a key transcription factor for uterine corin expression in pregnancy. In cultured human uterine endometrial cells, KLF17 binds to the CORIN promoter and enhances the promoter activity. Disruption of the KLF17 gene in the endometrial cells abolishes CORIN expression. In mice, Klf17 is up-regulated in the pregnant uterus. Klf17 deficiency prevents uterine Corin expression in pregnancy. Moreover, Klf17-deficient mice have poorly remodeled uterine spiral arteries and develop gestational hypertension and proteinuria. Together, our results reveal an important function of KLF17 in regulating Corin expression and uterine physiology in pregnancy.

螺旋动脉重塑是怀孕子宫中的重要生理过程，会增加流向胎儿的血液。螺旋动脉重构受损会导致先兆子痫，这是妊娠的主要疾病。Corin是一种跨膜丝氨酸蛋白酶，在妊娠子宫中被上调，以促进螺旋动脉重构。迄今为止，子宫皮质蛋白上调的潜在机制仍然未知。在这里，我们显示Krüppel样因子（KLF）17是怀孕时子宫corin表达的关键转录因子。在培养的人子宫内膜细胞中，KLF17与CORIN启动子结合并增强启动子活性。子宫内膜细胞中KLF17基因的破坏消除了CORIN表达。在小鼠中，Klf17在怀孕的子宫中被上调。Klf17缺乏症可阻止妊娠期子宫Corin表达。此外，Klf17缺陷型小鼠的子宫螺旋动脉重构较差，并产生了妊娠高血压和蛋白尿。总之，我们的结果揭示了KLF17在调节妊娠期Corin表达和子宫生理中的重要功能。