Role of estrogen receptors in thyroid toxicity induced by mono (2-ethylhexyl) phthalate via endoplasmic reticulum stress: An in vitro mechanistic investigation |
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| Affiliation: | 1. Department of Occupational and Environmental Health, School of Public Health, Jilin University, Changchun, China;2. Faculty of Public Health, Pyongyang Medical University, Pyongyang, Democratic People''s Republic of Korea;1. Reproductive Medicine Center, Department of Obstetrics and Gynecology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China;2. NHC Key Laboratory of Study on Abnormal Gametes and Reproductive Tract (Anhui Medical University), Hefei, Anhui, China;3. Key Laboratory of Population Health Across Life Cycle (Anhui Medical University), Ministry of Education of the People’s Republic of China, Hefei, Anhui, China;4. Department of Oncology of The First Affiliated Hospital, the CAS Key Laboratory of Innate Immunity and Chronic Disease, Division of Life Science and Medicine, University of Science and Technology of China, Hefei, Anhui, China;5. Hefei National Laboratory for Physical Sciences at Microscale, School of Life Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China;6. Anhui Province Key Laboratory of Reproductive Health and Genetics, Hefei, Anhui, China;7. Biopreservation and Artificial Organs, Anhui Provincial Engineering Research Center, Anhui Medical University, Hefei, Anhui, China;1. Aquatic Toxicology Lab, Department of Zoology, Guru Nanak Dev University, Amritsar, Punjab 143005, India;2. Department of Biosciences, University Institute of Biotechnology, Chandigarh University, Punjab 140413, India;3. Molecular Microbiology Lab, Department of Molecular Biology and Biochemistry, Guru Nanak Dev University, Amritsar, Punjab 143005, India;1. Department of Occupational and Environmental Health, The University of Iowa, Iowa City, IA 52242, United States;2. Interdisciplinary Graduate Program in Human Toxicology, The University of Iowa, Iowa City, IA 52242, United States;3. IIHR Hydroscience and Engineering, The University of Iowa, Iowa City, IA 52242, United States;4. Department of Civil and Environmental Engineering, The University of Iowa, Iowa City, IA 52242, United States;5. Center for Health Effects of Environmental Contamination, The University of Iowa, Iowa City, IA 52242;1. Department of Biochemistry, Faculty of Science, Mahidol University, Bangkok Thailand;2. Department of Pathobiology, Faculty of Science, Mahidol University, Bangkok Thailand;1. Academic of Chemical Engineering, Universidade Tecnológica Federal do Paraná (UTFPR), Campus Francisco Beltrão, Paraná, Brazil;2. Academic Department of Agricultural Sciences, Universidade Tecnológica Federal do Paraná (UTFPR), Campus Francisco Beltrão, Francisco Beltrão, Paraná, Brazil;3. Academic Department of Physics, Statistics and Mathematics, Universidade Tecnológica Federal do Paraná (UTFPR), Francisco Beltrão, Paraná, Brazil;4. Academic Department of Engineering, Universidade Tecnológica Federal do Paraná (UTFPR), Campus Francisco Beltrão, Francisco Beltrão, Paraná, Brazil;5. Academic Department of Chemistry and Biology, Universidade Tecnológica Federal do Paraná (UTFPR), Campus Francisco Beltrão, Paraná, Brazil |
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| Abstract: | Mono(2-ethylhexyl) phthalate (MEHP) can influence the expression of estrogen receptors (ERs) and induce thyroid injury. The expression of ERs can be related to thyroid disease and abnormal expression of ERs has been associated with activation of endoplasmic reticulum stress. This study aimed to clarify the role of ERs in MEHP-induced thyroid damage via endoplasmic reticulum stress. We exposed Nthy-ori 3–1 cells to different doses of MEHP. We found that after the exposure, the cell viability and the expression levels of thyroid hormone metabolism-related proteins decreased, while the apoptosis level and the expression levels of ERs (ERα and GPR30) increased. Three endoplasmic reticulum stress-related signaling pathways were activated by MEHP. After ERα and GPR30 were knocked down, these three pathways were inhibited and the thyroid toxicity was alleviated. Taken together, our results indicate that MEHP can induce thyroid toxicity by upregulating the expression of ERs, further activating endoplasmic reticulum stress. |
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| Keywords: | MEHP Endoplasmic reticulum stress Estrogen receptors Thyroid toxicity |
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