生物
螺旋动脉
子宫内
祖细胞
胎盘循环
细胞生物学
内皮干细胞
胎盘
祖细胞
子宫动脉
内科学
解剖
内分泌学
干细胞
胎儿
怀孕
妊娠期
体外
遗传学
医学
作者
Bin Tan,Li Lin,Yu Yuan,Yao Long,Yi‐No Kang,Biao Huang,Lifei Huang,Jianhua Li,Chao Tong,Hongbo Qi
标识
DOI:10.1016/j.devcel.2024.04.009
摘要
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 play a role in the vascular injury-repair program is largely unexplored during remodeling. Here, we observe that preeclampsia-afflicted uterine spiral arteries 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 AMP-activated protein kinase (AMPK)-deficient endothelial progenitor cells through the inhibition of HO-1, damages residual endothelium and leads to the accumulation of extracellular matrix produced by vascular smooth muscle cells during remodeling, which is 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. This mechanism holds promise in elucidating the pathogenesis of preeclampsia.
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