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Role of LAMA4 Gene in Regulating Extravillous Trophoblasts in Pathogenesis of Preeclampsia
BACKGROUND: Preeclampsia is a severe obstetric complication affecting the health of pregnant women. The aim of this study was to determine the effect of LAMA4 gene on extravillous trophoblasts (EVTs) in the pathogenesis of preeclampsia and its possible regulatory mechanism. MATERIAL/METHODS: HTR-8/S...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Scientific Literature, Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6929560/ https://www.ncbi.nlm.nih.gov/pubmed/31842202 http://dx.doi.org/10.12659/MSM.917402 |
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author | Ji, Yingli Zhou, La Wang, Guijuan Qiao, Yanni Tian, Yuyu Feng, Yu |
author_facet | Ji, Yingli Zhou, La Wang, Guijuan Qiao, Yanni Tian, Yuyu Feng, Yu |
author_sort | Ji, Yingli |
collection | PubMed |
description | BACKGROUND: Preeclampsia is a severe obstetric complication affecting the health of pregnant women. The aim of this study was to determine the effect of LAMA4 gene on extravillous trophoblasts (EVTs) in the pathogenesis of preeclampsia and its possible regulatory mechanism. MATERIAL/METHODS: HTR-8/SVneo cells were transfected with small-interfering ribonucleic acid (siRNA) targeting LAMA. The LAMA4 protein level was detected via Western blotting. Moreover, the influences of LAMA4 gene on the proliferation, migration and invasion of HTR-8/SVneo cells were detected via cell counting kit-8 (CCK-8) assay and Transwell assay. We also assessed the influences of LAMA4 gene on vascular endothelial growth factor (VEGF) and soluble fms-like tyrosine kinase-1 (sFlt-1) messenger RNA (mRNA) levels in HTR-8/SVneo cells as measured by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: The cell lines with downregulation of LAMA4 gene were successfully established by transfection. Compared with those in the normal group, the proliferation, migration, and invasion of HTR-8/SVneo cells declined, the VEGF mRNA level was reduced, and the sFlt-1 mRNA level was increased in the silencing group. CONCLUSIONS: Downregulation of the LAMA4 gene inhibits the proliferation, migration, and invasion of EVT to suppress the expression of vascular factors, leading to the occurrence or development of preeclampsia. Our data provide new insights into modulation of LAMA4 expression as a potential target for therapy against preeclampsia. Further research is needed on placenta sampling from pre-eclamptic pregnancies to validate the effect of LAMA4 expression compared to control pregnancies. |
format | Online Article Text |
id | pubmed-6929560 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | International Scientific Literature, Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-69295602019-12-26 Role of LAMA4 Gene in Regulating Extravillous Trophoblasts in Pathogenesis of Preeclampsia Ji, Yingli Zhou, La Wang, Guijuan Qiao, Yanni Tian, Yuyu Feng, Yu Med Sci Monit Lab/In Vitro Research BACKGROUND: Preeclampsia is a severe obstetric complication affecting the health of pregnant women. The aim of this study was to determine the effect of LAMA4 gene on extravillous trophoblasts (EVTs) in the pathogenesis of preeclampsia and its possible regulatory mechanism. MATERIAL/METHODS: HTR-8/SVneo cells were transfected with small-interfering ribonucleic acid (siRNA) targeting LAMA. The LAMA4 protein level was detected via Western blotting. Moreover, the influences of LAMA4 gene on the proliferation, migration and invasion of HTR-8/SVneo cells were detected via cell counting kit-8 (CCK-8) assay and Transwell assay. We also assessed the influences of LAMA4 gene on vascular endothelial growth factor (VEGF) and soluble fms-like tyrosine kinase-1 (sFlt-1) messenger RNA (mRNA) levels in HTR-8/SVneo cells as measured by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: The cell lines with downregulation of LAMA4 gene were successfully established by transfection. Compared with those in the normal group, the proliferation, migration, and invasion of HTR-8/SVneo cells declined, the VEGF mRNA level was reduced, and the sFlt-1 mRNA level was increased in the silencing group. CONCLUSIONS: Downregulation of the LAMA4 gene inhibits the proliferation, migration, and invasion of EVT to suppress the expression of vascular factors, leading to the occurrence or development of preeclampsia. Our data provide new insights into modulation of LAMA4 expression as a potential target for therapy against preeclampsia. Further research is needed on placenta sampling from pre-eclamptic pregnancies to validate the effect of LAMA4 expression compared to control pregnancies. International Scientific Literature, Inc. 2019-12-16 /pmc/articles/PMC6929560/ /pubmed/31842202 http://dx.doi.org/10.12659/MSM.917402 Text en © Med Sci Monit, 2019 This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) ) |
spellingShingle | Lab/In Vitro Research Ji, Yingli Zhou, La Wang, Guijuan Qiao, Yanni Tian, Yuyu Feng, Yu Role of LAMA4 Gene in Regulating Extravillous Trophoblasts in Pathogenesis of Preeclampsia |
title | Role of LAMA4 Gene in Regulating Extravillous Trophoblasts in Pathogenesis of Preeclampsia |
title_full | Role of LAMA4 Gene in Regulating Extravillous Trophoblasts in Pathogenesis of Preeclampsia |
title_fullStr | Role of LAMA4 Gene in Regulating Extravillous Trophoblasts in Pathogenesis of Preeclampsia |
title_full_unstemmed | Role of LAMA4 Gene in Regulating Extravillous Trophoblasts in Pathogenesis of Preeclampsia |
title_short | Role of LAMA4 Gene in Regulating Extravillous Trophoblasts in Pathogenesis of Preeclampsia |
title_sort | role of lama4 gene in regulating extravillous trophoblasts in pathogenesis of preeclampsia |
topic | Lab/In Vitro Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6929560/ https://www.ncbi.nlm.nih.gov/pubmed/31842202 http://dx.doi.org/10.12659/MSM.917402 |
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