Maternal Diet-Induced Obesity Compromises Oxidative Stress Status and Angiogenesis in the Porcine Placenta by Upregulating Nox2 Expression

• Published in: Oxidative medicine and cellular longevity 2019, Vol.2019 (2019), p.1-13
• Main Authors: Yin, Yulong, Xie, Zhengjun, Tan, Chengquan, Deng, Jinping, Li, Qiqi, Yang, Linfang, Cheng, Chuanhui, Wang, Hao, Li, Jiaying, Yang, Yunyu, Hu, Chengjun, Liang, Zuman
• Format: Article
• Language: English
• Subjects: Adenosine Triphosphate - metabolism; Analysis; Angiogenesis; Animals; Animals, Newborn; Birth weight; Body mass index; Body weight; Diet; Energy; Fatty acids; Feeding Behavior; Female; Medical research; Mitochondrial DNA; NADPH Oxidase 2 - metabolism; NADPH Oxidase 4 - genetics; NADPH Oxidase 4 - metabolism; Neovascularization, Physiologic - genetics; Obesity; Obesity - enzymology; Obesity - pathology; Organelle Biogenesis; Oxidases; Oxidative Stress; Placenta; Placenta - blood supply; Placenta - enzymology; Placenta - pathology; Platelet Endothelial Cell Adhesion Molecule-1 - metabolism; Pregnancy; RNA; RNA, Messenger - genetics; RNA, Messenger - metabolism; Swine; Triglycerides; Up-Regulation; Vascular endothelial growth factor; von Willebrand Factor - metabolism
• ISSN: 1942-0900; 1942-0994
• DOI: 10.1155/2019/2481592

Maternal obesity is associated with placental oxidative stress. However, the mechanism underlying this association remains poorly understood. In the present study, a gilt obesity model was developed by exposure to different energy diets and used to investigate the role of NADPH oxidase 2 (Nox2) in the placenta. Specifically, 99 gilts (Guangdong Small-ear Spotted pig) at day 60 of gestation were randomly assigned to one of the following three treatments: low-energy group (L, DE=11.50 MJ/kg), medium-energy group (M, DE=12.41 MJ/kg), and high-energy group (H, DE=13.42 MJ/kg), with 11 replicate pens per treatment and 3 gilts per pen. At the start of the study, maternal body weight and backfat thickness were not significantly different in the three treatments. After the study, data indicated that the H group had higher body weight and backfat thickness gain for gilts during gestation and lower piglet birth weight compared with the other two groups. Additionally, the H group showed glucolipid metabolic disorders and increased triglyceride and nonesterified fatty acid contents in the placenta of gilts. Compared with the L group, the H group exhibited lower mitochondrial biogenesis and increased oxidative damage in the placenta. Importantly, increased mRNA expression and protein abundance of Nox2 were observed for the first time in H group placentae. Furthermore, compared with the L group, the H group showed a decrease in the density of placental vessels and the protein levels of vascular endothelial cadherin (VE-cadherin), vascular endothelial growth factor A (VEGF-A), and phosphorylation of vascular endothelial growth factor receptor 2 (p-VEGFR2) as well as the immunostaining intensity of platelet endothelial cell adhesion molecule-1 (CD31). Our findings suggest that maternal high-energy diet-induced obesity increases placental oxidative stress and decreases placental angiogenesis possibly through the upregulation of Nox2.