Tissue & cell · 2026
Study on the mechanism of DLK1 in placenta of intrahepatic cholestasis of pregnancy.
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Li Zhizun, Huang Xiaomei, Shao Yong, Tang Qin
Аннотация
BACKGROUND: Intrahepatic cholestasis of pregnancy (ICP) is a pregnancy-specific disorder, prominently characterized by elevated serum bile acids and adverse fetal outcomes. This study focused on the expression of Delta-like 1(DLK1) in the placenta of patients with ICP,along with the alterations in placental blood vessels and function. The bile acid - induced ICP cell model was utilized to clarify the impact of DLK1 on the function of trophoblast cells under the pathological context of ICP.
METHODS: Human placental tissues were subjected to immunohistochemical staining, immunofluorescence, Western blotting (WB)and qPCR. These techniques were employed to analyze the expression of DLK1 and functional status of blood vessels in the ICP placenta. An ICP cell model was established using Taurocholate acid (TCA). WB, qPCR, and reactive oxygen species (ROS) assays were conducted to detect the effects of TCA and DLK1 on trophoblast function. The effects of TCA and DLK1 on endothelial cell function were evaluated through migration and tube formation assays.
RESULTS: The results indicated that the expression levels of DLK1, placental growth factor, and angiogenesis factor were significantly lower in the human ICP placenta. Concomitantly, the Notch1 signaling pathway was found to be inhibited. The addition of DLK1 to the ICP cell model improved the function of the cells, and the supernatant of the trophoblast cells also promoted the migration and tube formation ability of HUVECs.
CONCLUSIONS: In the ICP placenta, the expression of DLK1 is reduced, accompanied by a decline in placental blood vessels and placental function. Exogenous addition of DLK1 can activate the Notch1 pathway, promote placental angiogenesis and mitigate oxidative damage.
METHODS: Human placental tissues were subjected to immunohistochemical staining, immunofluorescence, Western blotting (WB)and qPCR. These techniques were employed to analyze the expression of DLK1 and functional status of blood vessels in the ICP placenta. An ICP cell model was established using Taurocholate acid (TCA). WB, qPCR, and reactive oxygen species (ROS) assays were conducted to detect the effects of TCA and DLK1 on trophoblast function. The effects of TCA and DLK1 on endothelial cell function were evaluated through migration and tube formation assays.
RESULTS: The results indicated that the expression levels of DLK1, placental growth factor, and angiogenesis factor were significantly lower in the human ICP placenta. Concomitantly, the Notch1 signaling pathway was found to be inhibited. The addition of DLK1 to the ICP cell model improved the function of the cells, and the supernatant of the trophoblast cells also promoted the migration and tube formation ability of HUVECs.
CONCLUSIONS: In the ICP placenta, the expression of DLK1 is reduced, accompanied by a decline in placental blood vessels and placental function. Exogenous addition of DLK1 can activate the Notch1 pathway, promote placental angiogenesis and mitigate oxidative damage.