Xiaoheng Li1, Leping Ye1, Yufei Ge2, Kaiming Yuan1, Yufei Zhang3, Yong Liang4, Jia Wei1, Connie Zhao2, Qing-Quan Lian1, Xueqiong Zhu5, Ren-Shan Ge6. 1. The Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, China. 2. The Population Council & the Rockefeller University, 1230 York Avenue, New York, NY 10065, USA. 3. Heilongjiang Key Laboratory of Anti-fibrosis Biotherapy, Mudanjiang Medical University, Heilongjiang 157011, PR China. 4. Department of Oncology, The Affiliated Taizhou Municipal Hospital, Taizhou University, 381 Zhongshan East Road, Jiaojiang District, Taizhou City, Zhejiang Province, 318000, PR China. 5. The Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, China. Electronic address: wzzxq@wzhealth.com. 6. The Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, China; The Population Council & the Rockefeller University, 1230 York Avenue, New York, NY 10065, USA. Electronic address: r_ge@yahoo.com.
Abstract
OBJECTIVES: The objective of the present study is to investigate the mechanism of perfluorooctane sulfonate-induced low body weight of fetus by analysis of glucocorticoid metabolizing enzyme 11β-hydroxysteroid dehydrogenase 2 and gene expression profiling of the placenta after in utero PFOS exposure. STUDY DESIGN: Pregnant Sprague-Dawley dams were gavaged with 0, 5, and 20 mg/kg body weight PFOS daily from gestational day 12-18. On gestational day 18, pregnant dams were euthanized, placentas, and fetuses were collected. MAIN OUTCOME MEASURES: Body weights of fetuses and placentas were measured, the corticosterone levels in fetal serum, and 11β-hydroxysteroid dehydrogenase 2 as well as the placental gene profiling were analyzed. RESULTS: 20 mg/kg PFOS significantly reduced fetal body weight and placental weight. Both 5 and 20 mg/kg PFOS increased fetal serum corticosterone levels. PFOS potently inhibited placental 11β-hydroxysteroid dehydrogenase 2 activity. Of 21,910 genes, 45 genes were significantly downregulated ≥2 fold by 20 mg/kg PFOS, including extracellular matrix (Slpi and Pi16), growth factors and hormones (Trh and Pdf), ion transporters (Aqp1, S100a4, and Abp1), signal transducers (Kap and Ampd3), and structural constituents (A2m and Des). CONCLUSIONS: PFOS exposure may alter placental development and function, causing intrauterine growth restriction via inhibiting placental 11β-hydroxysteroid dehydrogenase 2.
OBJECTIVES: The objective of the present study is to investigate the mechanism of perfluorooctane sulfonate-induced low body weight of fetus by analysis of glucocorticoid metabolizing enzyme 11β-hydroxysteroid dehydrogenase 2 and gene expression profiling of the placenta after in utero PFOS exposure. STUDY DESIGN: Pregnant Sprague-Dawley dams were gavaged with 0, 5, and 20 mg/kg body weight PFOS daily from gestational day 12-18. On gestational day 18, pregnant dams were euthanized, placentas, and fetuses were collected. MAIN OUTCOME MEASURES: Body weights of fetuses and placentas were measured, the corticosterone levels in fetal serum, and 11β-hydroxysteroid dehydrogenase 2 as well as the placental gene profiling were analyzed. RESULTS: 20 mg/kg PFOS significantly reduced fetal body weight and placental weight. Both 5 and 20 mg/kg PFOS increased fetal serum corticosterone levels. PFOS potently inhibited placental 11β-hydroxysteroid dehydrogenase 2 activity. Of 21,910 genes, 45 genes were significantly downregulated ≥2 fold by 20 mg/kg PFOS, including extracellular matrix (Slpi and Pi16), growth factors and hormones (Trh and Pdf), ion transporters (Aqp1, S100a4, and Abp1), signal transducers (Kap and Ampd3), and structural constituents (A2m and Des). CONCLUSIONS:PFOS exposure may alter placental development and function, causing intrauterine growth restriction via inhibiting placental 11β-hydroxysteroid dehydrogenase 2.
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