PI3K signaling pathway plays a significant role in embryonic stem cells (ES cells) self-renewal. Overexpression of Nanog maintains mouse ES cells pluripotency independent of leukemia inhibitory factor (LIF). However, little is known about the effect of PI3K signaling pathway on ES cells with Nanog overexpression. Our experiments aimed to explore the relationship between PI3K signaling pathway and Nanog expression in ES cells. We observed the effect of LY294002, a specific inhibitor of PI3K pathway, on wild-type J1 cells and Nanog overexpressing (Ex-Nanog) J1 cells in the presence or absence of LIF. With LY294002 treatment, both of them lost their ES features even in the presence of LIF. But the differentiation induced by LY294002 on Ex-Nanog J1 cells was slighter lower than that on wild-type J1 cells. These results indicate that inhibition of PI3K pathway induces mouse ES cells differentiation. Exogenous Nanog sustains mouse ES cells pluripotency independent of LIF, and alleviates the differentiation induced by LY294002. But it is insufficient to totally reverse the differentiation.
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Department of Biochemistry, Faculty of Pharmacy, Badr University in Cairo (BUC), Badr City, , 11829, Cairo, Egypt.
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Department of Physiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
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College of Biology and Food Engineering, Chongqing Three Gorges University, Chongqing, 404100, China.
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Huadong Medical Institute of Biotechniques, Nanjing, China.
Acetaminophen induced acute liver injury (ALI) has a high incidence and is a serious medical problem, but there is a lack of effective treatment. The enterohepatic axis is one of the targets of recent attention due to its important role in liver diseases. Disulfiram (DSF) is a multitarget drug that has been proven to play a role in a variety of liver diseases and can affect intestinal flora, but whether it can alleviate ALI is not clear.
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Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Fetal growth restriction (FGR) is characterized by the inability of the fetus to achieve its growth potential due to pathological factors, most commonly impaired placental trophoblast cell function. Currently, effective prevention and treatment methods of FGR are limited. We aimed to explore the pathogenesis of FGR and provide potential strategies for mitigating its occurrence.
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