Loss of placental growth factor ameliorates maternal hypertension and preeclampsia in mice

• Published in: The Journal of clinical investigation Vol. 128; no. 11; pp. 5008 - 5017
• Main Authors: Parchem, Jacqueline G, Kanasaki, Keizo, Kanasaki, Megumi, Sugimoto, Hikaru, Xie, Liang, Hamano, Yuki, Lee, Soo Bong, Gattone, Vincent H, Parry, Samuel, Strauss, Jerome F, Garovic, Vesna D, McElrath, Thomas F, Lu, Karen H, Sibai, Baha M, LeBleu, Valerie S, Carmeliet, Peter, Kalluri, Raghu
• Format: Journal Article
• Language: English
• Published: United States American Society for Clinical Investigation 01.11.2018
• Subjects: Angiogenesis; Animals; Biomedical research; Blood Pressure; Catechol; Catechol O-methyltransferase; Complications; Disease Models, Animal; Female; Genotype & phenotype; Glycogen; Glycogen - genetics; Glycogen - metabolism; Hypertension; Hypoxia; Ischemia; Kinases; Metabolism; Methyltransferase; Mice; Mice, Knockout; Models, Biological; Pathogenesis; Placenta; Placenta - metabolism; Placenta - pathology; Placenta Growth Factor - deficiency; Pre-eclampsia; Pre-Eclampsia - genetics; Pre-Eclampsia - metabolism; Pre-Eclampsia - pathology; Preeclampsia; Pregnancy; Protein-tyrosine kinase; Vascular endothelial growth factor; Vascular Endothelial Growth Factor Receptor-1 - genetics; Vascular Endothelial Growth Factor Receptor-1 - metabolism; Veins & arteries; Microcirculation; Carbohydrate metabolism; Reproductive Biology

Preeclampsia remains a clinical challenge due to its poorly understood pathogenesis. A prevailing notion is that increased placental production of soluble fms-like tyrosine kinase-1 (sFlt-1) causes the maternal syndrome by inhibiting proangiogenic placental growth factor (PlGF) and VEGF. However, th...