open access

Vol 88, No 7 (2017)
Research paper
Published online: 2017-07-31
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Study of the relationship between AGEs and oxidative stress damage to trophoblast cell mitochondria

Lingling Jiang1, Jianying Yan1, Lixiang Wu1
·
Pubmed: 28819942
·
Ginekol Pol 2017;88(7):372-378.
Affiliations
  1. Fujian Provincial Maternity and Children’s Hospital of Fujian Medical University, Fuzhou, Fujian, China, China

open access

Vol 88, No 7 (2017)
ORIGINAL PAPERS Obstetrics
Published online: 2017-07-31

Abstract

Objectives: To study the influence of AGEs on placental trophoblast mitochondria oxidative stress, and to explore the possible pathogenesis which may participate in pre-eclampsia.

Material and methods: Human trophoblast cells from early pregnancy were cultured by an enzyme-digestion method. When trophoblast cells reached approximately 70–80% after passages, they were incubated with pre-eclampsia serum for 24 hours. A fluorescent dye assay was applied to measure the mitochondrial membrane potential; ELISA was used to measure the activity of the mitochondrial permeability transition pore. mtDNA was detected by Real-time fluorescence quantitative Reverse Transcription-Polymerase Chain Reaction (RT-PCR). We continued to culture one group of cells with pre-eclampsia maternal serum, and other cells were pulsed with 600 mg/L AGEs. Cells were incubated for 16 hours before assaying the levels of mitochondrial oxidative stress damage.

Results: The levels of mitochondria oxidative stress damage in the AGEs group were higher than in the pre-eclampsia group 1 and pre-eclampsia group 2. There was no statistically significant difference in mitochondrial oxidative stress damage between the pre-eclampsia group 1 and group 2.

Conclusions: The AGEs are involved in the pathogenesis of pre-eclampsia, possibly through the enhancement of mito­chondrial oxidative stress damage.

Abstract

Objectives: To study the influence of AGEs on placental trophoblast mitochondria oxidative stress, and to explore the possible pathogenesis which may participate in pre-eclampsia.

Material and methods: Human trophoblast cells from early pregnancy were cultured by an enzyme-digestion method. When trophoblast cells reached approximately 70–80% after passages, they were incubated with pre-eclampsia serum for 24 hours. A fluorescent dye assay was applied to measure the mitochondrial membrane potential; ELISA was used to measure the activity of the mitochondrial permeability transition pore. mtDNA was detected by Real-time fluorescence quantitative Reverse Transcription-Polymerase Chain Reaction (RT-PCR). We continued to culture one group of cells with pre-eclampsia maternal serum, and other cells were pulsed with 600 mg/L AGEs. Cells were incubated for 16 hours before assaying the levels of mitochondrial oxidative stress damage.

Results: The levels of mitochondria oxidative stress damage in the AGEs group were higher than in the pre-eclampsia group 1 and pre-eclampsia group 2. There was no statistically significant difference in mitochondrial oxidative stress damage between the pre-eclampsia group 1 and group 2.

Conclusions: The AGEs are involved in the pathogenesis of pre-eclampsia, possibly through the enhancement of mito­chondrial oxidative stress damage.

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Keywords

pre-eclampsia, advanced glycation end products, oxidative stress, trophoblast cell

About this article
Title

Study of the relationship between AGEs and oxidative stress damage to trophoblast cell mitochondria

Journal

Ginekologia Polska

Issue

Vol 88, No 7 (2017)

Article type

Research paper

Pages

372-378

Published online

2017-07-31

Page views

1494

Article views/downloads

1375

DOI

10.5603/GP.a2017.0070

Pubmed

28819942

Bibliographic record

Ginekol Pol 2017;88(7):372-378.

Keywords

pre-eclampsia
advanced glycation end products
oxidative stress
trophoblast cell

Authors

Lingling Jiang
Jianying Yan
Lixiang Wu

References (15)
  1. Chekir C, Nakatsuka M, Noguchi S, et al. Accumulation of advanced glycation end products in women with preeclampsia: possible involvement of placental oxidative and nitrative stress. Placenta. 2006; 27(2-3): 225–233.
  2. Remor AP, de Matos FJ, Ghisoni K, et al. Differential effects of insulin on peripheral diabetes-related changes in mitochondrial bioenergetics: involvement of advanced glycosylated end products. Biochim Biophys Acta. 2011; 1812(11): 1460–1471.
  3. Yoshimaru T, Suzuki Y, Inoue T, et al. Extracellular superoxide released from mitochondria mediates mast cell death by advanced glycation end products. Biochim Biophys Acta. 2008; 1783(12): 2332–2343.
  4. Zusterzeel PL, Rütten H, Roelofs HM, et al. Protein carbonyls in decidua and placenta of pre-eclamptic women as markers for oxidative stress. Placenta. 2001; 22(2-3): 213–219.
  5. Leveno KJ, Cunningham FG, Gant NF. Williams manual of obstetrics, 21st edition. McGraw-Hill 2003.
  6. Bierhaus A, Illmer T, Kasper M, et al. Advanced glycation end product (AGE)-mediated induction of tissue factor in cultured endothelial cells is dependent on RAGE. Circulation. 1997; 96(7): 2262–2271.
  7. Liu HP, Wang RG, Li CM. Establishment of in vitro culture system of human archae-generation trophoblasts. Practical Preventive Medicine. 2006; 13(5): 1109–1111.
  8. Cha KY, Lee SH, Chung HM, et al. Quantification of mitochondrial DNA using real-time polymerase chain reaction in patients with premature ovarian failure. Fertil Steril. 2005; 84(6): 1712–1718.
  9. Oliver EA, Buhimschi CS, Dulay AT, et al. Activation of the receptor for advanced glycation end products system in women with severe preeclampsia. J Clin Endocrinol Metab. 2011; 96(3): 689–698.
  10. Guedes-Martins L, Matos L, Soares A, et al. AGEs, contributors to placental bed vascular changes leading to preeclampsia. Free Radic Res. 2013; 47 Suppl 1: 70–80.
  11. Loor G, Kondapalli J, Iwase H, et al. Mitochondrial oxidant stress triggers cell death in simulated ischemia-reperfusion. Biochim Biophys Acta. 2011; 1813(7): 1382–1394.
  12. Fang XY, Li YG, Lin NY. Mitochondrial permeability transition pore and its mechanism of influence by the mitochondrial ATP-sensitive potassium channel opening. Journal of Shantou University Medical College. 2012; 25(1): 61–64.
  13. Yan Jy, Xu X. [Relationships between concentrations of free fatty acid in serum and oxidative-damage levels in placental mitochondria and preeclampsia]. Zhonghua Fu Chan Ke Za Zhi. 2012; 47(6): 412–417.
  14. Yu SY, Huang L, Song MB. Increased reactive oxygen species in endothelial cells stimulated by advanced glycation end products mediated by NADPH oxidase. Chinese Journal of Arteriosclerosis. 2008; 16(11): 857–860.
  15. Huang QT, Zhang M, Zhong M, et al. Advanced glycation end products as an upstream molecule triggers ROS-induced sFlt-1 production in extravillous trophoblasts: a novel bridge between oxidative stress and preeclampsia. Placenta. 2013; 34(12): 1177–1182.

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