Abstract
IntroductionEmbryo implantation depends on trophoblast cells migration and invasion. Abnormal function of trophoblast cells could result in many pregnancy complications. Secreted protein acidic and rich in cysteine like-1 (SPARCL1) has been reported to inhibit cell migration and tumor invasion. This study aimed to explore the role of SPARCL1 in trophoblast functions. MethodsVillous specimens were obtained from 31 women with spontaneous abortion and 31 women with normal early pregnancy to determine the expression of SPARCL1. HTR8/SVneo cells and JAR cells were transfected with pIRES2-EGFP-SPARCL1 vectors and control vectors. The proliferation assay and scratch-wound assay were performed. Quantitative polymerase chain reaction (qPCR) and western blotting were performed to assess epithelial mesenchymal transition (EMT)-related molecules including MMP2, MMP3, N-cadherin, E-cadherin and vimentin. Extracellular signal-regulated kinase (ERK) phosphorylation activity and AP-1 expression in HTR8/SVneo cells following multi-scratching were detected using above assays. ResultsThe mRNA and protein levels of SPARCL1 were significantly higher in the abortion group than in the normal pregnancy group. After transfection, there was no difference of cell viability between the SPARCL1-overexpression group and control vector group. However, the migration distance and area were reduced and the abundances of EMT related molecules were changed by SPARCL1 overexpression when compared with controls. Lower ERK phosphorylation activity and decreased Fos and Jun expressions were noted at high level of SPARCL1. ConclusionRestrained migration and invasion were noted in trophoblast cells with SPARCL1 overexpression, which might affect embryo implantation and placenta development. It could be involved in the pathogenesis of spontaneous abortion.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
