Jun Tao1, Lin-Zhen Xia1, Jiao-Jiao Chen1, Jun-Fa Zeng1, Jun Meng2, ShiYuan Wu3, Zuo Wang1. 1. Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Disease, Hengyang Medical College, University of South China, Hengyang, China. 2. Functional Department, The First Affiliated Hospital of University of South China, Hengyang, China. 3. YueYang Maternal-Child Medicine Health Hospital, Hunan Province Innovative Training Base for Medical Postgraduates, Yueyang, China.
Abstract
AIM: This study aimed to investigate the effect of high glucose (HG) level on the proliferation, migration and invasion of trophoblasts and determine the role of placental growth factor (PLGF) in the process. METHODS: HTR8-S/Vneo was treated with different concentrations of d-glucose (0, 10, 15, 20, 25 and 30 μM) at different times (0, 6, 12 and 24 h). qRT-PCR and Western blot analyses were used to measure PLGF expression. The protein level of PLGF was measured by immunofluorescence. Cell proliferation was assessed with CCK-8 analysis. Wound healing and transwell assays were used to evaluate cell migration and invasion. Intercellular ROS was detected with DCFH-DA. RESULTS: After d-glucose treatment, the viability decreased in 25 and 30 μM groups. The HG group (25 μM) showed inhibited cell migration and invasion ability. The mRNA and protein levels of PLGF decreased under HG condition. Elevated ROS production was also detected in the HG group. Knocked-down PLGF expression enhanced increased ROS production and decreased cell migration and invasion, which reverted to the original levels after PLGF was overexpressed. CONCLUSION: High glucose treatment inhibited HTR8-S/Vneo viability, migration and invasion by downregulating PLGF expression.
AIM: This study aimed to investigate the effect of high glucose (HG) level on the proliferation, migration and invasion of trophoblasts and determine the role of placental growth factor (PLGF) in the process. METHODS: HTR8-S/Vneo was treated with different concentrations of d-glucose (0, 10, 15, 20, 25 and 30 μM) at different times (0, 6, 12 and 24 h). qRT-PCR and Western blot analyses were used to measure PLGF expression. The protein level of PLGF was measured by immunofluorescence. Cell proliferation was assessed with CCK-8 analysis. Wound healing and transwell assays were used to evaluate cell migration and invasion. Intercellular ROS was detected with DCFH-DA. RESULTS: After d-glucose treatment, the viability decreased in 25 and 30 μM groups. The HG group (25 μM) showed inhibited cell migration and invasion ability. The mRNA and protein levels of PLGF decreased under HG condition. Elevated ROS production was also detected in the HG group. Knocked-down PLGF expression enhanced increased ROS production and decreased cell migration and invasion, which reverted to the original levels after PLGF was overexpressed. CONCLUSION: High glucose treatment inhibited HTR8-S/Vneo viability, migration and invasion by downregulating PLGF expression.