| Description |
Placental ischemia, resulting from inadequate remodeling of uterine spiral arteries, is a factor in the development of preeclampsia. However, the effect of endothelial progenitor cells that plays a role in the vascular injury-repair program is largely unexplored during remodeling. Here, we observe that preeclampsia-afflicted uterine spiral arteries exhibit transition to a synthetic phenotype in vascular smooth muscle cells and characterize the regulatory axis in endothelial progenitor cells during remodeling in human decidua basalis. Excessive sEng, secreted by AMPK-deficient endothelial progenitor cells through the inhibition of HO-1, damages residual endothelium and leads to accumulation of extracellular matrix produced by vascular smooth muscle cells during remodeling, which are further confirmed by animal models. Collectively, our findings suggest that the impaired functionality of endothelial progenitor cells contributes to the narrowing of remodeled uterine spiral arteries, leading to reduced utero-placental perfusion, a mechanism that holds promise in elucidating the pathogenesis of preeclampsia. |
