Saturated and unsaturated fatty acids differentially regulate in vitro and ex vivo placental antioxidant capacity

Clarence R. Manuel, Maureen J. Charron, Charles R. Ashby, Sandra E. Reznik

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Problem: Complications from prematurity are the leading cause of death among children under 5 years of age. Although clinical studies have shown a positive correlation between maternal high-fat diet (HFD) and preterm birth (PTB), the underlying mechanisms remain to be elucidated. Furthermore, it remains unclear how fatty acid type influences the effects of bacterial endotoxins. Method of study: HTR-8/SVneo trophoblasts were cultured in either 0.5 mmol L-1 palmitic acid (PA) or linoleic acid (LA) in the absence or presence of 100 μg mL-1 of lipopolysaccharide (LPS) or lipoteichoic acid (LTA). Murine placental explants were cultured in either 2 mmol L-1 PA or LA, and cell viability, total antioxidant capacity (TAC), lipid peroxidation, H2O2, heme oxygenase-1 (HO-1), and nuclear erythroid 2-related factor 2 (Nrf-2) and nuclear factor-kappa light-chain enhancer of activated B cells (NF-κB) transcription factor activity assays were assessed. Results: Palmitic acid significantly (i) increased cell death, (ii) decreased TAC, and (iii) increased lipid peroxidation; but did not significantly increase HO-1. In contrast, LA maintained cell viability and significantly increased TAC and HO-1. In addition, incubating placental explants with PA significantly increased NF-κB activity. Co-incubating cells with PA and LPS or LTA significantly potentiated H2O2 production and increased lipid peroxidation. Co-incubating cells with PA and LTA synergistically impaired TAC, and LTA decreased TAC more so than LPS. Co-incubation with PA/LA and LPS/LTA decreased HO-1 levels compared to treatment with either fatty acid alone. Conclusion: Our findings suggest that saturated and unsaturated fats differentially regulate placental viability, antioxidant capacity, and inflammation and the actions of gram-positive and gram-negative endotoxins.

Original languageEnglish (US)
JournalAmerican Journal of Reproductive Immunology
DOIs
StateAccepted/In press - Jan 1 2018

Fingerprint

Palmitic Acid
Unsaturated Fatty Acids
Fatty Acids
Antioxidants
Heme Oxygenase-1
Linoleic Acid
Lipopolysaccharides
Lipid Peroxidation
Endotoxins
Cell Survival
Unsaturated Fats
Premature Birth
Trophoblasts
High Fat Diet
In Vitro Techniques
Cause of Death
B-Lymphocytes
Cell Death
Transcription Factors
Mothers

Keywords

  • Fatty acids
  • High-fat diet
  • Oxidative stress
  • Placental explants
  • Preterm birth
  • Trophoblasts

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Reproductive Medicine
  • Obstetrics and Gynecology

Cite this

Saturated and unsaturated fatty acids differentially regulate in vitro and ex vivo placental antioxidant capacity. / Manuel, Clarence R.; Charron, Maureen J.; Ashby, Charles R.; Reznik, Sandra E.

In: American Journal of Reproductive Immunology, 01.01.2018.

Research output: Contribution to journalArticle

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abstract = "Problem: Complications from prematurity are the leading cause of death among children under 5 years of age. Although clinical studies have shown a positive correlation between maternal high-fat diet (HFD) and preterm birth (PTB), the underlying mechanisms remain to be elucidated. Furthermore, it remains unclear how fatty acid type influences the effects of bacterial endotoxins. Method of study: HTR-8/SVneo trophoblasts were cultured in either 0.5 mmol L-1 palmitic acid (PA) or linoleic acid (LA) in the absence or presence of 100 μg mL-1 of lipopolysaccharide (LPS) or lipoteichoic acid (LTA). Murine placental explants were cultured in either 2 mmol L-1 PA or LA, and cell viability, total antioxidant capacity (TAC), lipid peroxidation, H2O2, heme oxygenase-1 (HO-1), and nuclear erythroid 2-related factor 2 (Nrf-2) and nuclear factor-kappa light-chain enhancer of activated B cells (NF-κB) transcription factor activity assays were assessed. Results: Palmitic acid significantly (i) increased cell death, (ii) decreased TAC, and (iii) increased lipid peroxidation; but did not significantly increase HO-1. In contrast, LA maintained cell viability and significantly increased TAC and HO-1. In addition, incubating placental explants with PA significantly increased NF-κB activity. Co-incubating cells with PA and LPS or LTA significantly potentiated H2O2 production and increased lipid peroxidation. Co-incubating cells with PA and LTA synergistically impaired TAC, and LTA decreased TAC more so than LPS. Co-incubation with PA/LA and LPS/LTA decreased HO-1 levels compared to treatment with either fatty acid alone. Conclusion: Our findings suggest that saturated and unsaturated fats differentially regulate placental viability, antioxidant capacity, and inflammation and the actions of gram-positive and gram-negative endotoxins.",
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AU - Ashby, Charles R.

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N2 - Problem: Complications from prematurity are the leading cause of death among children under 5 years of age. Although clinical studies have shown a positive correlation between maternal high-fat diet (HFD) and preterm birth (PTB), the underlying mechanisms remain to be elucidated. Furthermore, it remains unclear how fatty acid type influences the effects of bacterial endotoxins. Method of study: HTR-8/SVneo trophoblasts were cultured in either 0.5 mmol L-1 palmitic acid (PA) or linoleic acid (LA) in the absence or presence of 100 μg mL-1 of lipopolysaccharide (LPS) or lipoteichoic acid (LTA). Murine placental explants were cultured in either 2 mmol L-1 PA or LA, and cell viability, total antioxidant capacity (TAC), lipid peroxidation, H2O2, heme oxygenase-1 (HO-1), and nuclear erythroid 2-related factor 2 (Nrf-2) and nuclear factor-kappa light-chain enhancer of activated B cells (NF-κB) transcription factor activity assays were assessed. Results: Palmitic acid significantly (i) increased cell death, (ii) decreased TAC, and (iii) increased lipid peroxidation; but did not significantly increase HO-1. In contrast, LA maintained cell viability and significantly increased TAC and HO-1. In addition, incubating placental explants with PA significantly increased NF-κB activity. Co-incubating cells with PA and LPS or LTA significantly potentiated H2O2 production and increased lipid peroxidation. Co-incubating cells with PA and LTA synergistically impaired TAC, and LTA decreased TAC more so than LPS. Co-incubation with PA/LA and LPS/LTA decreased HO-1 levels compared to treatment with either fatty acid alone. Conclusion: Our findings suggest that saturated and unsaturated fats differentially regulate placental viability, antioxidant capacity, and inflammation and the actions of gram-positive and gram-negative endotoxins.

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