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The PI3K/Akt and ERK pathways elevate thyroid hormone receptor β1 and TRH receptor to decrease thyroid hormones after

Changjiang Liu1, Lianbing Li2, Mei Ha3

  • 1MOE Key Lab of Environment and Health, Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China; Key Lab of Birth Defects and Reproductive Health of National Health and Family Planning Commission, Chongqing Population and Family Planning Science and Technology Research Institute, Chongqing 400020, PR China.

Chemosphere
|October 4, 2014
PubMed
Summary

Polychlorinated biphenyls (PCBs) and DDT disrupt thyroid hormone (TH) homeostasis by activating PI3K/Akt and ERK pathways. These pathways alter TH receptors, disrupting the hypothalamic-pituitary-thyroid axis and lowering TH levels.

Keywords:
ERKPCB153PI3K/AktThyroid hormone receptor β1Thyrotropin releasing hormone receptorp,p′-DDE

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Area of Science:

  • Environmental Toxicology
  • Endocrinology
  • Molecular Biology

Background:

  • PCBs and DDT are environmental contaminants known to disrupt thyroid hormone (TH) homeostasis in humans and animals.
  • The precise molecular mechanisms underlying TH imbalance induced by these pollutants are not fully understood.
  • Signaling pathways like PI3K/Akt and MAPK are implicated in cellular responses to environmental stressors.

Purpose of the Study:

  • To investigate the role of PI3K/Akt and MAPK pathways in TH imbalance caused by PCB153 and p,p'-DDE exposure.
  • To elucidate the molecular mechanisms by which these signaling pathways mediate the disruption of the hypothalamic-pituitary-thyroid (HPT) axis.

Main Methods:

  • Sprague-Dawley rats were administered PCB153 and p,p'-DDE intraperitoneally for five consecutive days.
  • Human thyroid follicular epithelial cells (Nthy-ori 3-1) were treated with PCB153 and p,p'-DDE in vitro.
  • Serum levels of thyroid hormones (TT4, FT4, TT3, FT3) and pituitary/hypothalamic hormones (TSH, TRH) were measured.
  • Activation of PI3K/Akt and ERK pathways, and expression of TH receptors (TRβ1, TRα1) and TRH receptor (TRHr) were analyzed.

Main Results:

  • Exposure to PCB153 and p,p'-DDE decreased serum TT4, FT4, TT3, and TSH levels.
  • The PI3K/Akt and ERK pathways were activated both in vivo and in vitro following exposure.
  • Activated PI3K/Akt pathway led to elevated TRβ1, while activated ERK pathway increased TRHr expression.
  • Inhibition of PI3K/Akt decreased TRβ1, and inhibition of ERK decreased TRHr, confirming pathway involvement.

Conclusions:

  • Activated PI3K/Akt and ERK signaling pathways are key mediators in the disruption of the HPT axis by PCBs and DDT.
  • These pathways influence TH homeostasis by modulating the expression of TRβ1 and TRHr.
  • The findings suggest a potential molecular mechanism for how PCBs and DDT disturb thyroid hormone balance.