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Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure on acetylcholinesterase during myogenic differentiation of contractile rat primary skeletal muscle cells.

Abstract

Emerging data indicate that prenatal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) could interfere with myogenic differentiation in vivo. Acetylcholinesterase (EC3.1.1.7; AChE), an enzyme critical for cholinergic neurotransmission, is abundantly expressed in neurons and mature myotubes, and we recently found that muscle AChE expression was suppressed in parallel with the inhibition of myogenic differentiation upon TCDD treatment in mouse C2C12 cells. This TCDD-induced suppression of muscle AChE was proposed to involve an aryl hydrocarbon receptor (AhR)-independent mechanism, but the precise underlying mechanism remains unclear. Considering the widely recognized role of muscular activity in AChE expression and its potential crosstalk with the AhR signaling pathway, we sought to investigate the effect of TCDD on muscle AChE expression in the presence of muscular activity. Therefore, we employed a highly contractile rat primary skeletal muscle culture system in which AChE activity and the expression of genes related to it (AChE T subunit and collagen Q (ColQ)) were increased during the myogenic differentiation process. Although TCDD treatment successfully induced the expression of genes regulated by AhR activation, the treatment exerted no notable effects on myogenic differentiation. Moreover, muscle AChE enzymatic activity and mRNA level remained unchanged following TCDD treatment, and only ColQ mRNA expression was slightly increased after 4-day treatment with TCDD (10-10 M). The compensatory role of muscle-contraction-related signaling pathways in this newly identified unresponsiveness of muscle AChE to TCDD warrants further investigation.

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  • Authors+Show Affiliations

    ,

    State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center of Eco-Environment Sciences, Chinese Academy of Sciences, Beijing, 100085, China; University of Chinese Academy of Sciences, Beijing, China.

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    State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center of Eco-Environment Sciences, Chinese Academy of Sciences, Beijing, 100085, China; University of Chinese Academy of Sciences, Beijing, China. Electronic address: qhxie@rcees.ac.cn.

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    State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center of Eco-Environment Sciences, Chinese Academy of Sciences, Beijing, 100085, China; University of Chinese Academy of Sciences, Beijing, China.

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    State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center of Eco-Environment Sciences, Chinese Academy of Sciences, Beijing, 100085, China; Division of Life Science and Center for Chinese Medicine, the Hong Kong University of Science and Technology, Hong Kong, Hong Kong.

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    State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center of Eco-Environment Sciences, Chinese Academy of Sciences, Beijing, 100085, China; University of Chinese Academy of Sciences, Beijing, China.

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    State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center of Eco-Environment Sciences, Chinese Academy of Sciences, Beijing, 100085, China; University of Chinese Academy of Sciences, Beijing, China.

    ,

    State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center of Eco-Environment Sciences, Chinese Academy of Sciences, Beijing, 100085, China; University of Chinese Academy of Sciences, Beijing, China.

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    State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center of Eco-Environment Sciences, Chinese Academy of Sciences, Beijing, 100085, China; University of Chinese Academy of Sciences, Beijing, China.

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    State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center of Eco-Environment Sciences, Chinese Academy of Sciences, Beijing, 100085, China; University of Chinese Academy of Sciences, Beijing, China.

    ,

    Division of Life Science and Center for Chinese Medicine, the Hong Kong University of Science and Technology, Hong Kong, Hong Kong.

    State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center of Eco-Environment Sciences, Chinese Academy of Sciences, Beijing, 100085, China; University of Chinese Academy of Sciences, Beijing, China. Electronic address: binzhao@rcees.ac.cn.

    Source

    Chemico-biological interactions 308: 2019 May 14 pg 164-169

    Pub Type(s)

    Journal Article

    Language

    eng

    PubMed ID

    31100272

    Citation

    Luo, Yali, et al. "Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin Exposure On Acetylcholinesterase During Myogenic Differentiation of Contractile Rat Primary Skeletal Muscle Cells." Chemico-biological Interactions, vol. 308, 2019, pp. 164-169.
    Luo Y, Xie HQ, Chen Y, et al. Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure on acetylcholinesterase during myogenic differentiation of contractile rat primary skeletal muscle cells. Chem Biol Interact. 2019;308:164-169.
    Luo, Y., Xie, H. Q., Chen, Y., Xia, Y., Sha, R., Liu, Y., ... Zhao, B. (2019). Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure on acetylcholinesterase during myogenic differentiation of contractile rat primary skeletal muscle cells. Chemico-biological Interactions, 308, pp. 164-169. doi:10.1016/j.cbi.2019.05.018.
    Luo Y, et al. Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin Exposure On Acetylcholinesterase During Myogenic Differentiation of Contractile Rat Primary Skeletal Muscle Cells. Chem Biol Interact. 2019 May 14;308:164-169. PubMed PMID: 31100272.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure on acetylcholinesterase during myogenic differentiation of contractile rat primary skeletal muscle cells. AU - Luo,Yali, AU - Xie,Heidi Qunhui, AU - Chen,Yangsheng, AU - Xia,Yingjie, AU - Sha,Rui, AU - Liu,Yiyun, AU - Ma,Yongchao, AU - Xu,Tong, AU - Xu,Li, AU - Wah-Keung Tsim,Karl, AU - Zhao,Bin, Y1 - 2019/05/14/ PY - 2019/03/07/received PY - 2019/04/30/revised PY - 2019/05/13/accepted PY - 2019/5/18/pubmed PY - 2019/5/18/medline PY - 2019/5/18/entrez KW - Acetylcholinesterase KW - Aryl hydrocarbon receptor KW - Dioxin KW - Muscle contraction KW - Primary skeletal muscle cell SP - 164 EP - 169 JF - Chemico-biological interactions JO - Chem. Biol. Interact. VL - 308 N2 - Emerging data indicate that prenatal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) could interfere with myogenic differentiation in vivo. Acetylcholinesterase (EC3.1.1.7; AChE), an enzyme critical for cholinergic neurotransmission, is abundantly expressed in neurons and mature myotubes, and we recently found that muscle AChE expression was suppressed in parallel with the inhibition of myogenic differentiation upon TCDD treatment in mouse C2C12 cells. This TCDD-induced suppression of muscle AChE was proposed to involve an aryl hydrocarbon receptor (AhR)-independent mechanism, but the precise underlying mechanism remains unclear. Considering the widely recognized role of muscular activity in AChE expression and its potential crosstalk with the AhR signaling pathway, we sought to investigate the effect of TCDD on muscle AChE expression in the presence of muscular activity. Therefore, we employed a highly contractile rat primary skeletal muscle culture system in which AChE activity and the expression of genes related to it (AChE T subunit and collagen Q (ColQ)) were increased during the myogenic differentiation process. Although TCDD treatment successfully induced the expression of genes regulated by AhR activation, the treatment exerted no notable effects on myogenic differentiation. Moreover, muscle AChE enzymatic activity and mRNA level remained unchanged following TCDD treatment, and only ColQ mRNA expression was slightly increased after 4-day treatment with TCDD (10-10 M). The compensatory role of muscle-contraction-related signaling pathways in this newly identified unresponsiveness of muscle AChE to TCDD warrants further investigation. SN - 1872-7786 UR - https://www.unboundmedicine.com/medline/citation/31100272/Effect_of_2,3,7,8-tetrachlorodibenzo-p-dioxin_exposure_on_acetylcholinesterase_during_myogenic_differentiation_of_contractile_rat_primary_skeletal_muscle_cells L2 - https://linkinghub.elsevier.com/retrieve/pii/S0009-2797(19)30393-X DB - PRIME DP - Unbound Medicine ER -