Dysregulated GLUT1 results in the pathogenesis of preeclampsia by impairing the function of trophoblast cells

• Published in: Scientific reports 2024-10, Vol.14 (1), p.23761-14, Article 23761
• Main Authors: Pei, Jingyuan, Liao, Yangyou, Bai, Xiaoxian, Li, Min, Wang, Jing, Li, Xiaotong, Zhang, Hongshuo, Sui, Linlin, Kong, Ying
• Format: Article
• Language: English
• Subjects: 1-Phosphatidylinositol 3-kinase; 631/92; 692/420; 692/699; Adult; AKT protein; Cell Line; Cell migration; Cell Movement; Cell Proliferation; Female; Fetuses; Glucose; Glucose - metabolism; Glucose transport; Glucose transporter; Glucose Transporter Type 1 - genetics; Glucose Transporter Type 1 - metabolism; GLUT1; Humanities and Social Sciences; Humans; MAP kinase; Migration and invasion; Morbidity; multidisciplinary; Pathogenesis; Phosphatidylinositol 3-Kinases - metabolism; Placenta; Placenta - metabolism; Placenta - pathology; Pre-eclampsia; Pre-Eclampsia - metabolism; Pre-Eclampsia - pathology; Preeclampsia; Pregnancy; Pregnancy complications; Proliferation; Protein transport; Proto-Oncogene Proteins c-akt - metabolism; Science; Science (multidisciplinary); Signal Transduction; Syncytialization; Therapeutic targets; Trophoblast cells; Trophoblasts - metabolism; Trophoblasts - pathology
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-024-74489-z

Preeclampsia (PE) is a common placental-origin complication of pregnancy and a major cause of morbidity and mortality among pregnant women and fetuses. However, its pathogenesis has not been elucidated. Effective strategies for prevention, screening, and treatment are still lacking. Studies have indicated that dysfunction of placental trophoblast cells, such as impaired syncytialization, proliferation, and epithelial-mesenchymal transition processes, plays a crucial role in the development of PE. Glucose transporter 1 (GLUT1) is a key protein regulating glucose transport in placental tissues. However, the effect of GLUT1 on the function of trophoblast cells in PE is not well understood. In this study, we found that GLUT1 expression is reduced in PE placental tissues. GLUT1 promotes the syncytialization process by increasing the glucose uptake ability of BeWo cells. Additionally, GLUT1 promotes the proliferation, migration, and invasion capabilities of HTR-8/SVneo cells by regulating MAPK and PI3K/AKT signaling pathways. Overall, these findings provide a new insight into understanding the biological functions of GLUT1, clarifying the pathogenesis of PE, and identifying diagnostic and therapeutic targets for PE.