Environmental Pollutant Polybrominated Diphenyl Ether, a Flame Retardant, Induces Primary Amnion Cell Senescence

Faranak Behnia, Morgan R. Peltier, George Saade, Ramkumar Menon

    Research output: Contribution to journalArticle

    18 Citations (Scopus)

    Abstract

    Objective: Polybrominated diphenyl ethers (PBDEs) are documented to increase the risk for spontaneous preterm birth (PTB). We hypothesize that PBDEs cause oxidative stress (OS) that leads to fetal cell senescence and inflammation associated with PTB. Methods: Primary amnion epithelial cells (n = 5) isolated from term, not in labor pregnancies, were exposed to PBDE congeners 47 and 99 (each 5 μm). ROS kinetics was monitored. Morphologic changes, phospho-p38 MAPK (P-p38) activation, development of senescence, and induction of uterotonins (COX-2 expression) were quantified using light microscopy, Western blot, senescence-associated β-galactosidase (SA β-gal) staining, and qRT-PCR, respectively, after 48 and 72 hr of exposure. Results: Both PBDE congeners induced ROS within 2 min compared to controls (P < 0.05). P-p38 activation was significant after PBDE-99 treatment than controls (P < 0.05). After 72 hr of treatment, both PBDE-treated cells showed cell death-associated morphologic changes with significantly higher SA β-gal-stained cells than control. COX-2 expression was higher after 72 hr of treatment with PBDE-99. Overall, the PBDE-99 response was more pronounced than PBDE-47. Conclusions: Congener-dependent OS response, p38 MAPK activation, senescence, and COX-2 expression were seen in human amnion cells by PBDEs. These findings demonstrate environment pollutant-induced senescence activation and inflammation can lead to pathways resulting in PTB.

    Original languageEnglish (US)
    JournalAmerican Journal of Reproductive Immunology
    DOIs
    StateAccepted/In press - 2015

    Fingerprint

    Halogenated Diphenyl Ethers
    Flame Retardants
    Environmental Pollutants
    Amnion
    Cell Aging
    Premature Birth
    p38 Mitogen-Activated Protein Kinases
    Galactosidases
    Oxidative Stress
    Inflammation
    Microscopy
    Cell Death
    Western Blotting
    Epithelial Cells

    Keywords

    • Flame retardants
    • Persistent organic pollutants
    • Preterm birth
    • Sterile inflammation
    • Toxic chemicals

    ASJC Scopus subject areas

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

    Cite this

    @article{1ae72b277e0e445bba54c84787d3c073,
    title = "Environmental Pollutant Polybrominated Diphenyl Ether, a Flame Retardant, Induces Primary Amnion Cell Senescence",
    abstract = "Objective: Polybrominated diphenyl ethers (PBDEs) are documented to increase the risk for spontaneous preterm birth (PTB). We hypothesize that PBDEs cause oxidative stress (OS) that leads to fetal cell senescence and inflammation associated with PTB. Methods: Primary amnion epithelial cells (n = 5) isolated from term, not in labor pregnancies, were exposed to PBDE congeners 47 and 99 (each 5 μm). ROS kinetics was monitored. Morphologic changes, phospho-p38 MAPK (P-p38) activation, development of senescence, and induction of uterotonins (COX-2 expression) were quantified using light microscopy, Western blot, senescence-associated β-galactosidase (SA β-gal) staining, and qRT-PCR, respectively, after 48 and 72 hr of exposure. Results: Both PBDE congeners induced ROS within 2 min compared to controls (P < 0.05). P-p38 activation was significant after PBDE-99 treatment than controls (P < 0.05). After 72 hr of treatment, both PBDE-treated cells showed cell death-associated morphologic changes with significantly higher SA β-gal-stained cells than control. COX-2 expression was higher after 72 hr of treatment with PBDE-99. Overall, the PBDE-99 response was more pronounced than PBDE-47. Conclusions: Congener-dependent OS response, p38 MAPK activation, senescence, and COX-2 expression were seen in human amnion cells by PBDEs. These findings demonstrate environment pollutant-induced senescence activation and inflammation can lead to pathways resulting in PTB.",
    keywords = "Flame retardants, Persistent organic pollutants, Preterm birth, Sterile inflammation, Toxic chemicals",
    author = "Faranak Behnia and Peltier, {Morgan R.} and George Saade and Ramkumar Menon",
    year = "2015",
    doi = "10.1111/aji.12414",
    language = "English (US)",
    journal = "American Journal of Reproductive Immunology and Microbiology",
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    }

    TY - JOUR

    T1 - Environmental Pollutant Polybrominated Diphenyl Ether, a Flame Retardant, Induces Primary Amnion Cell Senescence

    AU - Behnia, Faranak

    AU - Peltier, Morgan R.

    AU - Saade, George

    AU - Menon, Ramkumar

    PY - 2015

    Y1 - 2015

    N2 - Objective: Polybrominated diphenyl ethers (PBDEs) are documented to increase the risk for spontaneous preterm birth (PTB). We hypothesize that PBDEs cause oxidative stress (OS) that leads to fetal cell senescence and inflammation associated with PTB. Methods: Primary amnion epithelial cells (n = 5) isolated from term, not in labor pregnancies, were exposed to PBDE congeners 47 and 99 (each 5 μm). ROS kinetics was monitored. Morphologic changes, phospho-p38 MAPK (P-p38) activation, development of senescence, and induction of uterotonins (COX-2 expression) were quantified using light microscopy, Western blot, senescence-associated β-galactosidase (SA β-gal) staining, and qRT-PCR, respectively, after 48 and 72 hr of exposure. Results: Both PBDE congeners induced ROS within 2 min compared to controls (P < 0.05). P-p38 activation was significant after PBDE-99 treatment than controls (P < 0.05). After 72 hr of treatment, both PBDE-treated cells showed cell death-associated morphologic changes with significantly higher SA β-gal-stained cells than control. COX-2 expression was higher after 72 hr of treatment with PBDE-99. Overall, the PBDE-99 response was more pronounced than PBDE-47. Conclusions: Congener-dependent OS response, p38 MAPK activation, senescence, and COX-2 expression were seen in human amnion cells by PBDEs. These findings demonstrate environment pollutant-induced senescence activation and inflammation can lead to pathways resulting in PTB.

    AB - Objective: Polybrominated diphenyl ethers (PBDEs) are documented to increase the risk for spontaneous preterm birth (PTB). We hypothesize that PBDEs cause oxidative stress (OS) that leads to fetal cell senescence and inflammation associated with PTB. Methods: Primary amnion epithelial cells (n = 5) isolated from term, not in labor pregnancies, were exposed to PBDE congeners 47 and 99 (each 5 μm). ROS kinetics was monitored. Morphologic changes, phospho-p38 MAPK (P-p38) activation, development of senescence, and induction of uterotonins (COX-2 expression) were quantified using light microscopy, Western blot, senescence-associated β-galactosidase (SA β-gal) staining, and qRT-PCR, respectively, after 48 and 72 hr of exposure. Results: Both PBDE congeners induced ROS within 2 min compared to controls (P < 0.05). P-p38 activation was significant after PBDE-99 treatment than controls (P < 0.05). After 72 hr of treatment, both PBDE-treated cells showed cell death-associated morphologic changes with significantly higher SA β-gal-stained cells than control. COX-2 expression was higher after 72 hr of treatment with PBDE-99. Overall, the PBDE-99 response was more pronounced than PBDE-47. Conclusions: Congener-dependent OS response, p38 MAPK activation, senescence, and COX-2 expression were seen in human amnion cells by PBDEs. These findings demonstrate environment pollutant-induced senescence activation and inflammation can lead to pathways resulting in PTB.

    KW - Flame retardants

    KW - Persistent organic pollutants

    KW - Preterm birth

    KW - Sterile inflammation

    KW - Toxic chemicals

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    U2 - 10.1111/aji.12414

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    JO - American Journal of Reproductive Immunology and Microbiology

    JF - American Journal of Reproductive Immunology and Microbiology

    SN - 1046-7408

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