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Low concentration of BPA induces mice spermatocytes apoptosis via GPR30
Bisphenol A (BPA) acts as xenoestrogen and has a great impact on disorders of human reproductive system. However, the mechanism through which BPA can affect human testicular function remains to be identified. GPR30 is a novel membrane estrogen receptor with high-affinity and low-capacity binding to...
Autores principales: | , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5564744/ https://www.ncbi.nlm.nih.gov/pubmed/28446726 http://dx.doi.org/10.18632/oncotarget.16923 |
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author | Wang, Chaoliang Zhang, Jianxiang Li, Qi Zhang, Tianbiao Deng, Zishi Lian, Jing Jia, Donghui Li, Rui Zheng, Tao Ding, Xiaoju Yang, Fan Ma, Chao Wang, Rui Zhang, Weixing Wen, Jian Guo |
author_facet | Wang, Chaoliang Zhang, Jianxiang Li, Qi Zhang, Tianbiao Deng, Zishi Lian, Jing Jia, Donghui Li, Rui Zheng, Tao Ding, Xiaoju Yang, Fan Ma, Chao Wang, Rui Zhang, Weixing Wen, Jian Guo |
author_sort | Wang, Chaoliang |
collection | PubMed |
description | Bisphenol A (BPA) acts as xenoestrogen and has a great impact on disorders of human reproductive system. However, the mechanism through which BPA can affect human testicular function remains to be identified. GPR30 is a novel membrane estrogen receptor with high-affinity and low-capacity binding to estrogens. We demonstrated that estrogen receptor α (ERα), estrogen receptor β (ERβ) as well as GPR30 are expressed in mouse spermatocyte-derived GC-2 cells using Real-time PCR. We treated the cells with different doses of BPA and found that even low doses of BPA can inhibit GC-2 cell growth using MTT assay. To make sure which receptor is responsible for the biological function of BPA, we used ER down-regulator ICI and indicated that BPA could bind to GPR30. We also observed that BPA was able to induce Erk1/2 phosphorylation in GC-2 cells and proved that this process was mediated by GPR30–related EGFR-MAPK pathway using western blot. By Real-time PCR, we found that the expression of c-Fos was up-regulated and Cyclin D1 gene was down-regulated, in the presence of BPA and ICI. The results of MTT assay, comet assay and flow cytometry indicated that the activation of GPR30 induced by BPA inhibited the cell growth and induced cell apoptosis and ICI, GPR30 siRNA, EGFR inhibitor (AG), and MAPK (PD) inhibitor could partially reverse this effect. Immunohistochemistry on the testis of BPA –damaged mice showed that BPA induced spermatocyte apoptosis without affecting the seminiferous tubules and spermatocyte. In conclusion, BPA triggered spermatocyte apoptosis via GPR30. |
format | Online Article Text |
id | pubmed-5564744 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-55647442017-08-23 Low concentration of BPA induces mice spermatocytes apoptosis via GPR30 Wang, Chaoliang Zhang, Jianxiang Li, Qi Zhang, Tianbiao Deng, Zishi Lian, Jing Jia, Donghui Li, Rui Zheng, Tao Ding, Xiaoju Yang, Fan Ma, Chao Wang, Rui Zhang, Weixing Wen, Jian Guo Oncotarget Research Paper Bisphenol A (BPA) acts as xenoestrogen and has a great impact on disorders of human reproductive system. However, the mechanism through which BPA can affect human testicular function remains to be identified. GPR30 is a novel membrane estrogen receptor with high-affinity and low-capacity binding to estrogens. We demonstrated that estrogen receptor α (ERα), estrogen receptor β (ERβ) as well as GPR30 are expressed in mouse spermatocyte-derived GC-2 cells using Real-time PCR. We treated the cells with different doses of BPA and found that even low doses of BPA can inhibit GC-2 cell growth using MTT assay. To make sure which receptor is responsible for the biological function of BPA, we used ER down-regulator ICI and indicated that BPA could bind to GPR30. We also observed that BPA was able to induce Erk1/2 phosphorylation in GC-2 cells and proved that this process was mediated by GPR30–related EGFR-MAPK pathway using western blot. By Real-time PCR, we found that the expression of c-Fos was up-regulated and Cyclin D1 gene was down-regulated, in the presence of BPA and ICI. The results of MTT assay, comet assay and flow cytometry indicated that the activation of GPR30 induced by BPA inhibited the cell growth and induced cell apoptosis and ICI, GPR30 siRNA, EGFR inhibitor (AG), and MAPK (PD) inhibitor could partially reverse this effect. Immunohistochemistry on the testis of BPA –damaged mice showed that BPA induced spermatocyte apoptosis without affecting the seminiferous tubules and spermatocyte. In conclusion, BPA triggered spermatocyte apoptosis via GPR30. Impact Journals LLC 2017-04-07 /pmc/articles/PMC5564744/ /pubmed/28446726 http://dx.doi.org/10.18632/oncotarget.16923 Text en Copyright: © 2017 Wang et al. http://creativecommons.org/licenses/by/3.0/ This article is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) (CC-BY), which permits unrestricted use and redistribution provided that the original author and source are credited. |
spellingShingle | Research Paper Wang, Chaoliang Zhang, Jianxiang Li, Qi Zhang, Tianbiao Deng, Zishi Lian, Jing Jia, Donghui Li, Rui Zheng, Tao Ding, Xiaoju Yang, Fan Ma, Chao Wang, Rui Zhang, Weixing Wen, Jian Guo Low concentration of BPA induces mice spermatocytes apoptosis via GPR30 |
title | Low concentration of BPA induces mice spermatocytes apoptosis via GPR30 |
title_full | Low concentration of BPA induces mice spermatocytes apoptosis via GPR30 |
title_fullStr | Low concentration of BPA induces mice spermatocytes apoptosis via GPR30 |
title_full_unstemmed | Low concentration of BPA induces mice spermatocytes apoptosis via GPR30 |
title_short | Low concentration of BPA induces mice spermatocytes apoptosis via GPR30 |
title_sort | low concentration of bpa induces mice spermatocytes apoptosis via gpr30 |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5564744/ https://www.ncbi.nlm.nih.gov/pubmed/28446726 http://dx.doi.org/10.18632/oncotarget.16923 |
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