CPT1A modulates PI3K/Akt/mTOR pathway to promote preeclampsia

作者全名："Chen, Miaomiao; Chao, Bingdi; Xu, Jiacheng; Liu, Zheng; Tao, Yuelan; He, Jie; Wang, Jie; Yang, Huan; Luo, Xin; Qi, Hongbo"

作者地址："[Chen, Miaomiao; Chao, Bingdi; Xu, Jiacheng; Liu, Zheng; Tao, Yuelan; He, Jie; Wang, Jie; Yang, Huan; Luo, Xin; Qi, Hongbo] Chongqing Med Univ, Affiliated Hosp 1, Dept Obstet & Gynecol, 1 Youyi Rd, Chongqing 400016, Peoples R China; [Chen, Miaomiao] Huazhong Univ Sci & Technol, Maternal & Child Hlth Hosp Hubei Prov, Affiliated Hosp, Tongji Med Coll,Dept Obstet, Wuhan 430070, Peoples R China; [Chen, Miaomiao; Chao, Bingdi; Xu, Jiacheng; Liu, Zheng; Tao, Yuelan; He, Jie; Wang, Jie; Yang, Huan; Luo, Xin; Qi, Hongbo] Chongqing Med Univ, China Canada New Zealand Joint Lab Maternal & Feta, 1 Yixueyuan Rd, Chongqing 400016, Peoples R China; [Qi, Hongbo] Chongqing Med Univ, Women & Childrens Hosp, Chongqing 401147, Peoples R China"

通信作者："Luo, X; Qi, HB (通讯作者)，Chongqing Med Univ, Affiliated Hosp 1, Dept Obstet & Gynecol, 1 Youyi Rd, Chongqing 400016, Peoples R China.; Luo, X; Qi, HB (通讯作者)，Chongqing Med Univ, China Canada New Zealand Joint Lab Maternal & Feta, 1 Yixueyuan Rd, Chongqing 400016, Peoples R China."

来源：PLACENTA

ESI学科分类：CLINICAL MEDICINE

WOS号：WOS:000964859300001

JCR分区：Q1

影响因子：3

年份：2023

卷号：133

期号：　

开始页：23

结束页：31

文献类型：Article

关键词：Preeclampsia; CPT1A; EMT; PI3K/Akt/mTOR pathway

摘要："Introduction: Preeclampsia (PE) refers to a syndrome of new-onset hypertension with multisystem involvement and damage after 20 weeks of gestation. Defective placentation due to dysregulated behaviors of trophoblast cells is considered a predominant cause of PE. Methods: Immunofluorescence (if) and Western blot were used to detect the expression and localization of Carnitine palmitoyltransferase 1A (CPT1A) in placenta. CPT1A protein was overexpressed/knocked down in HTR8/SVneo cells by lentiviral/siRNA interference method. CCK-8 Assay, Western blot, flow cytometry, Wound healing and Transwell assay were used to detect the functional impact of CPT1A on HTR8/SVneo cells. Transcriptomics and bioinformatics analysis were used to predict the possible pathway of CPT1A participating in PE. Results: CPT1A was upregulated in preeclamptic placentas when compared with normal controls. The abnormal expression of CPT1A in HTR8/SVneo cells is associated with the invasion and migration of HTR8/SVneo cells but is not related to the proliferation, cycle, and apoptosis of HTR8/SVneo cells. The results of Transcriptomic and Western blots suggest that phosphatidylinositol-3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway are activated in the si-CPT1A-1796 group. Compared with the si-NC group, the epithelial-mesenchymal transition (EMT) process of HTR8/SVneo cells in the si-CPT1A-1796 group was significantly enhanced. Discussion: CPT1A may participate in the pathogenesis of PE by inhibiting the EMT process of HTR8/SVneo cells through the PI3K/AKT/mTOR signaling axis. Thus, the newly unveiled novel function of CPT1A in PE via the PI3K/Akt/mTOR pathway provides a novel insight into the pathogenesis of PE."

基金机构："National Natural Science Foundation of China [82171668, 81771614, 82171662]; in-hospitalprograms of Maternal and Child Health Hospital of Hubei Province [2021SFYY001]"

基金资助正文："This work was supported by the National Natural Science Foundation of China (No. 82171668, No. 81771614, No. 82171662) and in-hospitalprograms of Maternal and Child Health Hospital of Hubei Province (No. 2021SFYY001) ."