Conclusion and implication
Our data indicate that 11β-HSD2 is a crucial factor for placental
development and maintaining balance release of pro- and anti-angiogenic
factors in placenta. We reveal previously unrecognized role of placental
11β-HSD2 dysfunction in the pathogenesis of PE and immediately highlight
innovative targets to counteract PE.
Keywords: preeclampsia; 11β-HSD2; glucocorticoids; ADAM17; placenta
Abbreviations:
11β-HSD, 11β-hydroxysteroid dehydrogenase; PE, preeclampsia; CBX,
carbenoxolone; sFlt1, fms-like tyrosine kinase 1; PlGF, placental growth
factor; ADAM, a disintegrin and metalloprotease; GC, glucocorticoids;
IUGR, intrauterine growth retardation; ICG, indocyanine green; ICG-NPs,
ICG-loaded nanoparticles; CSA, chondroitin sulfate A; ICG-CSA-NPs,
ICG-NPs linked to CSA binding peptide; CBX-NPs, CBX-loaded
nanoparticles; CBX-SCR, CBX-NPs linked to scramble peptide; CBX-CSA,
CBX-NPs linked to CSA binding peptide; NAD, nicotinamide adenine
dinucleotide; NADP, nicotinamide adenine dinucleotide phosphate; EVT,
extravillous cytotrophoblasts; GAPDH, glyceraldehyde-3-phosphate
dehydrogenase;
GD,
gestational day; BP, blood pressure; VEGF, vascular endothelial growth
factor; DEX, dexamethasone; MT, mesometrial triangle;
GREs, glucocorticoid response
elements; MMP, matrix metalloprotein; MAP, mean arterial pressure; TBC,
trophoblast; SA, spiral artery.