| http://purl.uniprot.org/citations/27770612 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/27770612 | http://www.w3.org/2000/01/rdf-schema#comment | "Autophagy, identified as type II programmed cell death, has already been known to be involved in the pathophysiology of preeclampsia (PE), which is a gestational disease with high morbidity. The present study aims to investigate the functional role of let-7i, a miRNA, in trophoblastic autophagy. Placental tissue used in this study was collected from patients with severe preeclampsia (SPE) or normal pregnant women. A decreased level of let-7i was found in placenta of SPE. In addition, autophagic vacuoles were observed in SPE and the expression of microtubule associated protein 1 light chain 3 (LC3) II/I was elevated. In vitro, let-7i mimics suppressed the autophagic activities in human HTR-8/SVneo trophoblast cell line (HTR-8) and human placental choriocarcinoma cell line JEG-3, whereas let-7i inhibitor enhanced the activities. As a potential target of let-7i, autophagy-related 4B cysteine peptidase (Atg4B) had an increased expression level in SPE. As expected, the increased expression of Atg4B was negatively regulated by let-7i using dual luciferase reporter assay. Furthermore, these trophoblast-like cells transfected with the let-7i mimic or inhibitors resulted in a significant change of Atg4B in both mRNA and protein level. More importantly, Atg4B overexpression could partly reverse let-7i mimic-reduced LC3II/I levels; whereas Atg4B silencing partly attenuated let-7i inhibitor-induced the level of LC3II/I expression. Taken together, these findings suggest that let-7i is able to regulate autophagic activity via regulating Atg4B expression, which might contribute to the pathogenesis of PE. J. Cell. Physiol. 232: 2581-2589, 2017. © 2016 Wiley Periodicals, Inc."xsd:string |
| http://purl.uniprot.org/citations/27770612 | http://purl.org/dc/terms/identifier | "doi:10.1002/jcp.25661"xsd:string |
| http://purl.uniprot.org/citations/27770612 | http://purl.uniprot.org/core/author | "Chen Y."xsd:string |
| http://purl.uniprot.org/citations/27770612 | http://purl.uniprot.org/core/author | "Huang X."xsd:string |
| http://purl.uniprot.org/citations/27770612 | http://purl.uniprot.org/core/author | "Wang L."xsd:string |
| http://purl.uniprot.org/citations/27770612 | http://purl.uniprot.org/core/author | "Xu Y."xsd:string |
| http://purl.uniprot.org/citations/27770612 | http://purl.uniprot.org/core/author | "Xie J."xsd:string |
| http://purl.uniprot.org/citations/27770612 | http://purl.uniprot.org/core/author | "Fu J."xsd:string |
| http://purl.uniprot.org/citations/27770612 | http://purl.uniprot.org/core/date | "2017"xsd:gYear |
| http://purl.uniprot.org/citations/27770612 | http://purl.uniprot.org/core/name | "J Cell Physiol"xsd:string |
| http://purl.uniprot.org/citations/27770612 | http://purl.uniprot.org/core/pages | "2581-2589"xsd:string |
| http://purl.uniprot.org/citations/27770612 | http://purl.uniprot.org/core/title | "Let-7i-Induced Atg4B Suppression Is Essential for Autophagy of Placental Trophoblast in Preeclampsia."xsd:string |
| http://purl.uniprot.org/citations/27770612 | http://purl.uniprot.org/core/volume | "232"xsd:string |
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