Bisphenol A exerts thyroid-hormone-like effects on mouse oligodendrocyte precursor cells

Chika Seiwa; Jin Nakahara; Takatsugu Komiyama; Yoshinao Katsu; Taisen Iguchi; Hiroaki Asou

doi:10.1159/000080663

Bisphenol A exerts thyroid-hormone-like effects on mouse oligodendrocyte precursor cells

Chika Seiwa, Jin Nakahara, Takatsugu Komiyama, Yoshinao Katsu, Taisen Iguchi, Hiroaki Asou

Research output: Contribution to journal › Article › peer-review

70 Citations (Scopus)

Abstract

We report studies on the mechanism of action of bisphenol A (BPA) on the differentiation of oligodendrocyte precursor cells (OPCs). Our results show that: (1) BPA inhibits the differentiation of OPCs induced by exposure to thyroid hormone (T₃ ). (2) The effect is mediated through various mechanisms via the thyroid hormone receptor (TRβ1) which is considered to be responsible for OPC differentiation. (3) The action of BPA on OPC differentiation does not involve the FcRγ -Fyn-myelin basic protein (MBP) cascade as an inducer of OPC differentiation nor does it suppress CREB phosphorylation, which is considered to be induced by the T₃ -TR complex. (4) The presence of MBP isoforms (21.5, 18.5, 17.0 and 14.0 kDa) was detected in OPCs, and the expression of exon 2-containing isoforms (i.e. 17.0 and 21.5 kDa) was upregulated upon treatment with T₃ . In contrast, expression of MBP was inhibited by BPA.

Original language	English
Pages (from-to)	21-30
Number of pages	10
Journal	Neuroendocrinology
Volume	80
Issue number	1
DOIs	https://doi.org/10.1159/000080663
Publication status	Published - 2004 Jan 1
Externally published	Yes

Keywords

Bisphenol
Gonadal hormones
Mice
Myelin basic proteins
Oligodendrocytes
Selective estrogen receptor modulators
Thyroid hormone receptors
Thyroid hormones

ASJC Scopus subject areas

Endocrinology, Diabetes and Metabolism
Endocrinology
Endocrine and Autonomic Systems
Cellular and Molecular Neuroscience

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1159/000080663

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abstract = "We report studies on the mechanism of action of bisphenol A (BPA) on the differentiation of oligodendrocyte precursor cells (OPCs). Our results show that: (1) BPA inhibits the differentiation of OPCs induced by exposure to thyroid hormone (T3 ). (2) The effect is mediated through various mechanisms via the thyroid hormone receptor (TRβ1) which is considered to be responsible for OPC differentiation. (3) The action of BPA on OPC differentiation does not involve the FcRγ -Fyn-myelin basic protein (MBP) cascade as an inducer of OPC differentiation nor does it suppress CREB phosphorylation, which is considered to be induced by the T3 -TR complex. (4) The presence of MBP isoforms (21.5, 18.5, 17.0 and 14.0 kDa) was detected in OPCs, and the expression of exon 2-containing isoforms (i.e. 17.0 and 21.5 kDa) was upregulated upon treatment with T3 . In contrast, expression of MBP was inhibited by BPA.",

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author = "Chika Seiwa and Jin Nakahara and Takatsugu Komiyama and Yoshinao Katsu and Taisen Iguchi and Hiroaki Asou",

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AU - Seiwa, Chika

AU - Nakahara, Jin

AU - Komiyama, Takatsugu

AU - Katsu, Yoshinao

AU - Iguchi, Taisen

AU - Asou, Hiroaki

PY - 2004/1/1

Y1 - 2004/1/1

N2 - We report studies on the mechanism of action of bisphenol A (BPA) on the differentiation of oligodendrocyte precursor cells (OPCs). Our results show that: (1) BPA inhibits the differentiation of OPCs induced by exposure to thyroid hormone (T3 ). (2) The effect is mediated through various mechanisms via the thyroid hormone receptor (TRβ1) which is considered to be responsible for OPC differentiation. (3) The action of BPA on OPC differentiation does not involve the FcRγ -Fyn-myelin basic protein (MBP) cascade as an inducer of OPC differentiation nor does it suppress CREB phosphorylation, which is considered to be induced by the T3 -TR complex. (4) The presence of MBP isoforms (21.5, 18.5, 17.0 and 14.0 kDa) was detected in OPCs, and the expression of exon 2-containing isoforms (i.e. 17.0 and 21.5 kDa) was upregulated upon treatment with T3 . In contrast, expression of MBP was inhibited by BPA.

AB - We report studies on the mechanism of action of bisphenol A (BPA) on the differentiation of oligodendrocyte precursor cells (OPCs). Our results show that: (1) BPA inhibits the differentiation of OPCs induced by exposure to thyroid hormone (T3 ). (2) The effect is mediated through various mechanisms via the thyroid hormone receptor (TRβ1) which is considered to be responsible for OPC differentiation. (3) The action of BPA on OPC differentiation does not involve the FcRγ -Fyn-myelin basic protein (MBP) cascade as an inducer of OPC differentiation nor does it suppress CREB phosphorylation, which is considered to be induced by the T3 -TR complex. (4) The presence of MBP isoforms (21.5, 18.5, 17.0 and 14.0 kDa) was detected in OPCs, and the expression of exon 2-containing isoforms (i.e. 17.0 and 21.5 kDa) was upregulated upon treatment with T3 . In contrast, expression of MBP was inhibited by BPA.

KW - Bisphenol

KW - Gonadal hormones

KW - Mice

KW - Myelin basic proteins

KW - Oligodendrocytes

KW - Selective estrogen receptor modulators

KW - Thyroid hormone receptors

KW - Thyroid hormones

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Bisphenol A exerts thyroid-hormone-like effects on mouse oligodendrocyte precursor cells

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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