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Pan Yibin,Yan Lili,Chen Qiaoqiao,Wei Cheng,Dai Yongdong,Tong Xiaomei,Zhu Haiyan,Lu Meifei,Zhang Yanling,Jin Xiaoying,Zhang Tai,Lin Xiaona,Zhou Feng,Zhang Songying 생화학분자생물학회 2021 Experimental and molecular medicine Vol.53 No.-
In early pregnancy, the placenta anchors the conceptus and supports embryonic development and survival. This study aimed to investigate the underlying functions of Shh signaling in recurrent miscarriage (RM), a serious disorder of pregnancy. In the present study, Shh and Gli2 were mainly observed in cytotrophoblasts (CTBs), Ptch was mainly observed in syncytiotrophoblasts (STBs), and Smo and Gli3 were expressed in both CTBs and STBs. Shh signaling was significantly impaired in human placenta tissue from recurrent miscarriage patients compared to that of gestational age-matched normal controls. VEGF-A and CD31 protein levels were also significantly decreased in recurrent miscarriage patients. Furthermore, inhibition of Shh signaling impaired the motility of JAR cells by regulating the expression of Gli2 and Gli3. Intriguingly, inhibition of Shh signaling also triggered autophagy and autolysosome accumulation. Additionally, knockdown of BECN1 reversed Gant61-induced motility inhibition. In conclusion, our results showed that dysfunction of Shh signaling activated autophagy to inhibit trophoblast motility, which suggests the Shh pathway and autophagy as potential targets for RM therapy.
Molecular mechanisms of 1,2-dichloroethane-induced neurotoxicity
Xiang Yang,Zhang Xiaoshun,Tian Zhiling,Cheng Yibin,Liu Ningguo,Meng Xiaojing 한국독성학회 2023 Toxicological Research Vol.39 No.4
The production of industrial solvents and adhesives often utilizes 1,2-dichloroethane (1,2-DCE), a highly toxic halogenated hydrocarbon compound. Occupational 1,2-DCE poisoning occurs frequently and is a public health concern. Exposure to 1,2-DCE can damage the brain, liver, and kidneys. The main and most severe damage caused by exposure to 1,2-DCE is to the nervous system, especially the central nervous system. Current research on 1,2-DCE mainly focuses on the mechanism of brain edema. Several possible mechanisms of 1,2-DCE neurotoxicity have been proposed, including oxidative stress, calcium overload, blood–brain barrier damage, and neurotransmitter changes. This article reviews the research progress on 1,2-DCE neurotoxicity and the mechanism behind it to provide a scientific basis for the prevention and treatment of 1,2-DCE poisoning.