Paternal Inheritance of Bisphenol A Cardiotoxic Effects: The Implications of Sperm Epigenome
Parental exposure to bisphenol A (BPA) has been linked to a greater incidence of congenital diseases. We have demonstrated that BPA induces in zebrafish males an increase in the acetylation of sperm histones that is transmitted to the blastomeres of the unexposed progeny. This work is aimed to deter...
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MDPI AG
2021-02-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/22/4/2125 |
| _version_ | 1797395765426913280 |
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| author | Marta Lombó María Paz Herráez |
| author_facet | Marta Lombó María Paz Herráez |
| author_sort | Marta Lombó |
| collection | DOAJ |
| description | Parental exposure to bisphenol A (BPA) has been linked to a greater incidence of congenital diseases. We have demonstrated that BPA induces in zebrafish males an increase in the acetylation of sperm histones that is transmitted to the blastomeres of the unexposed progeny. This work is aimed to determine whether histone hyperacetylation promoted by paternal exposure to BPA is the molecular mechanism underlying the cardiogenesis impairment in the descendants. Zebrafish males were exposed to 100 and 2000 µg/L BPA during early spermatogenesis and mated with non-exposed females. We analyzed in the progeny the expression of genes involved in cardiogenesis and the epigenetic profile. Once the histone hyperacetylation was confirmed, treatment with epigallocatechin gallate (EGCG), an inhibitor of histone acetyltransferases, was assayed on F1 embryos. Embryos from males exposed to 2000 µg/L BPA overexpressed the transcription factor <i>hand2</i> and the receptor <i>esr2b</i>, showing their own promoters—as well as that of <i>kat6a</i>—an enrichment in H3K9ac. In embryos treated with EGCG, both gene expression and histone acetylation (global and specific) returned to basal levels, and the phenotype was recovered. As shown by the results, the histone hyperacetylated landscape promoted by BPA in the sperm alters the chromatin structure of the progeny, leading to the overexpression of the histone acetyltransferase and genes involved in cardiogenesis. |
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| format | Article |
| id | doaj.art-3ae1eb2d9a3941b58b1b2ccc13be90e4 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-09T00:40:23Z |
| publishDate | 2021-02-01 |
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| series | International Journal of Molecular Sciences |
| spelling | doaj.art-3ae1eb2d9a3941b58b1b2ccc13be90e42023-12-11T17:51:28ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-02-01224212510.3390/ijms22042125Paternal Inheritance of Bisphenol A Cardiotoxic Effects: The Implications of Sperm EpigenomeMarta Lombó0María Paz Herráez1Department of Animal Reproduction, INIA, Avenida Puerta de Hierro, 18, 28040 Madrid, SpainDepartment of Molecular Biology, Faculty of Biology, University of León, Campus Vegazana s/n, 24071 León, SpainParental exposure to bisphenol A (BPA) has been linked to a greater incidence of congenital diseases. We have demonstrated that BPA induces in zebrafish males an increase in the acetylation of sperm histones that is transmitted to the blastomeres of the unexposed progeny. This work is aimed to determine whether histone hyperacetylation promoted by paternal exposure to BPA is the molecular mechanism underlying the cardiogenesis impairment in the descendants. Zebrafish males were exposed to 100 and 2000 µg/L BPA during early spermatogenesis and mated with non-exposed females. We analyzed in the progeny the expression of genes involved in cardiogenesis and the epigenetic profile. Once the histone hyperacetylation was confirmed, treatment with epigallocatechin gallate (EGCG), an inhibitor of histone acetyltransferases, was assayed on F1 embryos. Embryos from males exposed to 2000 µg/L BPA overexpressed the transcription factor <i>hand2</i> and the receptor <i>esr2b</i>, showing their own promoters—as well as that of <i>kat6a</i>—an enrichment in H3K9ac. In embryos treated with EGCG, both gene expression and histone acetylation (global and specific) returned to basal levels, and the phenotype was recovered. As shown by the results, the histone hyperacetylated landscape promoted by BPA in the sperm alters the chromatin structure of the progeny, leading to the overexpression of the histone acetyltransferase and genes involved in cardiogenesis.https://www.mdpi.com/1422-0067/22/4/2125bisphenol Apaternal exposurehistone acetylationsperm epigenomeheart development |
| spellingShingle | Marta Lombó María Paz Herráez Paternal Inheritance of Bisphenol A Cardiotoxic Effects: The Implications of Sperm Epigenome International Journal of Molecular Sciences bisphenol A paternal exposure histone acetylation sperm epigenome heart development |
| title | Paternal Inheritance of Bisphenol A Cardiotoxic Effects: The Implications of Sperm Epigenome |
| title_full | Paternal Inheritance of Bisphenol A Cardiotoxic Effects: The Implications of Sperm Epigenome |
| title_fullStr | Paternal Inheritance of Bisphenol A Cardiotoxic Effects: The Implications of Sperm Epigenome |
| title_full_unstemmed | Paternal Inheritance of Bisphenol A Cardiotoxic Effects: The Implications of Sperm Epigenome |
| title_short | Paternal Inheritance of Bisphenol A Cardiotoxic Effects: The Implications of Sperm Epigenome |
| title_sort | paternal inheritance of bisphenol a cardiotoxic effects the implications of sperm epigenome |
| topic | bisphenol A paternal exposure histone acetylation sperm epigenome heart development |
| url | https://www.mdpi.com/1422-0067/22/4/2125 |
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