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The relationship between free fatty acids and mitochondrial oxidative stress damage to trophoblast cell in preeclampsia
AIM: To investigate the effects of free fatty acids on mitochondrial oxidative stress and the pathogenesis of preeclampsia. METHODS: Human primary trophoblast cells at 6–8 weeks of gestation were retrieved and cultured to 70–80% confluence, then incubated in serum from women with a normal pregnancy...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8973543/ https://www.ncbi.nlm.nih.gov/pubmed/35361155 http://dx.doi.org/10.1186/s12884-022-04623-0 |
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author | Jiang, Lingling Yan, Jianying |
author_facet | Jiang, Lingling Yan, Jianying |
author_sort | Jiang, Lingling |
collection | PubMed |
description | AIM: To investigate the effects of free fatty acids on mitochondrial oxidative stress and the pathogenesis of preeclampsia. METHODS: Human primary trophoblast cells at 6–8 weeks of gestation were retrieved and cultured to 70–80% confluence, then incubated in serum from women with a normal pregnancy (normal pregnancy group), women with preeclampsia (PE group), and a combination of serum from women with 24 h preeclampsia-like symptoms and free fatty acids (FFA group). Mitochondrial membrane potential was assessed by fluorescent dye concurrent with detection of membrane channel conversion pore activity by fluorescence microscope. Enzyme labeling instruments and RT-PCR were used to detect mitochondrial DNA (mtDNA) levels. RESULTS: The preeclampsia and free fatty acids groups both exhibited significantly higher levels of mitochondria oxidative stress damage when compared to the normal pregnancy group. However, no significant differences in mitochondrial oxidative stress damage were observed between the FFA and PE groups. CONCLUSIONS: Serum free fatty acids might play an important role in the pathogenesis of preeclampsia by enhancing mitochondrial oxidative stress damage. |
format | Online Article Text |
id | pubmed-8973543 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-89735432022-04-02 The relationship between free fatty acids and mitochondrial oxidative stress damage to trophoblast cell in preeclampsia Jiang, Lingling Yan, Jianying BMC Pregnancy Childbirth Research AIM: To investigate the effects of free fatty acids on mitochondrial oxidative stress and the pathogenesis of preeclampsia. METHODS: Human primary trophoblast cells at 6–8 weeks of gestation were retrieved and cultured to 70–80% confluence, then incubated in serum from women with a normal pregnancy (normal pregnancy group), women with preeclampsia (PE group), and a combination of serum from women with 24 h preeclampsia-like symptoms and free fatty acids (FFA group). Mitochondrial membrane potential was assessed by fluorescent dye concurrent with detection of membrane channel conversion pore activity by fluorescence microscope. Enzyme labeling instruments and RT-PCR were used to detect mitochondrial DNA (mtDNA) levels. RESULTS: The preeclampsia and free fatty acids groups both exhibited significantly higher levels of mitochondria oxidative stress damage when compared to the normal pregnancy group. However, no significant differences in mitochondrial oxidative stress damage were observed between the FFA and PE groups. CONCLUSIONS: Serum free fatty acids might play an important role in the pathogenesis of preeclampsia by enhancing mitochondrial oxidative stress damage. BioMed Central 2022-03-31 /pmc/articles/PMC8973543/ /pubmed/35361155 http://dx.doi.org/10.1186/s12884-022-04623-0 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Jiang, Lingling Yan, Jianying The relationship between free fatty acids and mitochondrial oxidative stress damage to trophoblast cell in preeclampsia |
title | The relationship between free fatty acids and mitochondrial oxidative stress damage to trophoblast cell in preeclampsia |
title_full | The relationship between free fatty acids and mitochondrial oxidative stress damage to trophoblast cell in preeclampsia |
title_fullStr | The relationship between free fatty acids and mitochondrial oxidative stress damage to trophoblast cell in preeclampsia |
title_full_unstemmed | The relationship between free fatty acids and mitochondrial oxidative stress damage to trophoblast cell in preeclampsia |
title_short | The relationship between free fatty acids and mitochondrial oxidative stress damage to trophoblast cell in preeclampsia |
title_sort | relationship between free fatty acids and mitochondrial oxidative stress damage to trophoblast cell in preeclampsia |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8973543/ https://www.ncbi.nlm.nih.gov/pubmed/35361155 http://dx.doi.org/10.1186/s12884-022-04623-0 |
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