Di-n-butyl phthalate epigenetically induces reproductive toxicity via the PTEN/AKT pathway

Di-n-butyl phthalate (DBP) is a kind of ubiquitous chemical linked to hormonal disruptions that affects male reproductive system. However, the mechanism of DBP-induced germ cells toxicity remains unclear. Here, we demonstrate that DBP induces reduction of proliferation, increase of apoptosis and DNA...

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Published inCell death & disease Vol. 10; no. 4; p. 307
Main Authors Li, Ran, Xing, Qian-wei, Wu, Xiao-lu, Zhang, Lei, Tang, Min, Tang, Jing-yuan, Wang, Jing-zi, Han, Peng, Wang, Shang-qian, Wang, Wei, Zhang, Wei, Zhou, Guo-ping, Qin, Zhi-qiang
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 05.04.2019
Springer Nature B.V
Subjects
13/1
13/109
13/2
13/31
13/89
45/91
631/337/176/1988
631/80/82/23
AKT protein
Animals
Antibodies
Apoptosis
Apoptosis - drug effects
Biochemistry
Biomedical and Life Sciences
Cell Biology
Cell Culture
Cell Line
Cell Proliferation - drug effects
Demethylation
Dibutyl Phthalate - toxicity
DNA (Cytosine-5-)-Methyltransferases - genetics
DNA (Cytosine-5-)-Methyltransferases - metabolism
DNA damage
DNA Damage - drug effects
DNA Demethylation
DNA methylation
DNA Methyltransferase 3B
Flagella
Flagella - genetics
Flagella - metabolism
Germ cells
Immunology
Life Sciences
Male
Mice
Mice, Inbred C57BL
MicroRNAs - genetics
MicroRNAs - metabolism
n-Butyl phthalate
Promoter Regions, Genetic
Proto-Oncogene Proteins c-akt - antagonists & inhibitors
Proto-Oncogene Proteins c-akt - genetics
Proto-Oncogene Proteins c-akt - metabolism
PTEN Phosphohydrolase - chemistry
PTEN Phosphohydrolase - genetics
PTEN Phosphohydrolase - metabolism
PTEN protein
Reproductive system
Signal Transduction - drug effects
Sperm
Sperm Motility - drug effects
Sperm Motility - genetics
Spermatozoa - drug effects
Spermatozoa - metabolism
Testis - cytology
Testis - drug effects
Testis - metabolism
Toxicity
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Abstract Di-n-butyl phthalate (DBP) is a kind of ubiquitous chemical linked to hormonal disruptions that affects male reproductive system. However, the mechanism of DBP-induced germ cells toxicity remains unclear. Here, we demonstrate that DBP induces reduction of proliferation, increase of apoptosis and DNA damage dependent on the PTEN/AKT pathway. Mechanistically, DBP decreases PTEN promoter methylation and increases its transcriptional activity, leading to increased PTEN expression. Notably, DNMT3b is confirmed as a target of miR-29b and miR-29b-mediated status of PTEN methylation is involved in the effects of DBP treatment. Meanwhile, DBP decreases AKT pathway expression via increasing PTEN expression. In addition, the fact that DBP decreases the sperm number and the percentage of motile and progressive sperm is associated with downregulated AKT pathway and sperm flagellum-related genes. Collectively, these findings indicate that DBP induces aberrant PTEN demethylation, leading to inhibition of the AKT pathway, which contributes to the reproductive toxicity.
AbstractList Di-n-butyl phthalate (DBP) is a kind of ubiquitous chemical linked to hormonal disruptions that affects male reproductive system. However, the mechanism of DBP-induced germ cells toxicity remains unclear. Here, we demonstrate that DBP induces reduction of proliferation, increase of apoptosis and DNA damage dependent on the PTEN/AKT pathway. Mechanistically, DBP decreases PTEN promoter methylation and increases its transcriptional activity, leading to increased PTEN expression. Notably, DNMT3b is confirmed as a target of miR-29b and miR-29b-mediated status of PTEN methylation is involved in the effects of DBP treatment. Meanwhile, DBP decreases AKT pathway expression via increasing PTEN expression. In addition, the fact that DBP decreases the sperm number and the percentage of motile and progressive sperm is associated with downregulated AKT pathway and sperm flagellum-related genes. Collectively, these findings indicate that DBP induces aberrant PTEN demethylation, leading to inhibition of the AKT pathway, which contributes to the reproductive toxicity.
Di-n-butyl phthalate (DBP) is a kind of ubiquitous chemical linked to hormonal disruptions that affects male reproductive system. However, the mechanism of DBP-induced germ cells toxicity remains unclear. Here, we demonstrate that DBP induces reduction of proliferation, increase of apoptosis and DNA damage dependent on the PTEN/AKT pathway. Mechanistically, DBP decreases PTEN promoter methylation and increases its transcriptional activity, leading to increased PTEN expression. Notably, DNMT3b is confirmed as a target of miR-29b and miR-29b-mediated status of PTEN methylation is involved in the effects of DBP treatment. Meanwhile, DBP decreases AKT pathway expression via increasing PTEN expression. In addition, the fact that DBP decreases the sperm number and the percentage of motile and progressive sperm is associated with downregulated AKT pathway and sperm flagellum-related genes. Collectively, these findings indicate that DBP induces aberrant PTEN demethylation, leading to inhibition of the AKT pathway, which contributes to the reproductive toxicity.Di-n-butyl phthalate (DBP) is a kind of ubiquitous chemical linked to hormonal disruptions that affects male reproductive system. However, the mechanism of DBP-induced germ cells toxicity remains unclear. Here, we demonstrate that DBP induces reduction of proliferation, increase of apoptosis and DNA damage dependent on the PTEN/AKT pathway. Mechanistically, DBP decreases PTEN promoter methylation and increases its transcriptional activity, leading to increased PTEN expression. Notably, DNMT3b is confirmed as a target of miR-29b and miR-29b-mediated status of PTEN methylation is involved in the effects of DBP treatment. Meanwhile, DBP decreases AKT pathway expression via increasing PTEN expression. In addition, the fact that DBP decreases the sperm number and the percentage of motile and progressive sperm is associated with downregulated AKT pathway and sperm flagellum-related genes. Collectively, these findings indicate that DBP induces aberrant PTEN demethylation, leading to inhibition of the AKT pathway, which contributes to the reproductive toxicity.
ArticleNumber 307
Author Qin, Zhi-qiang
Wang, Shang-qian
Wang, Wei
Wang, Jing-zi
Zhang, Wei
Xing, Qian-wei
Wu, Xiao-lu
Tang, Min
Han, Peng
Li, Ran
Zhang, Lei
Zhou, Guo-ping
Tang, Jing-yuan
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  fullname: Wu, Xiao-lu
  organization: Department of Pediatrics, The First Affiliated Hospital of Nanjing Medical University
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  fullname: Zhang, Lei
  organization: Department of Urology, The First Affiliated Hospital of Nanjing Medical University
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  fullname: Tang, Min
  organization: Department of Urology, The First Affiliated Hospital of Nanjing Medical University
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  organization: Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine
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  organization: Department of Urology, The First Affiliated Hospital of Nanjing Medical University
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  organization: Department of Urology, The First Affiliated Hospital of Nanjing Medical University
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  fullname: Qin, Zhi-qiang
  email: qinzq_urology@sina.com
  organization: Department of Urology, Nanjing First Hospital, Nanjing Medical University
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Snippet Di-n-butyl phthalate (DBP) is a kind of ubiquitous chemical linked to hormonal disruptions that affects male reproductive system. However, the mechanism of...
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SubjectTerms 13/1
13/109
13/2
13/31
13/89
45/91
631/337/176/1988
631/80/82/23
AKT protein
Animals
Antibodies
Apoptosis
Apoptosis - drug effects
Biochemistry
Biomedical and Life Sciences
Cell Biology
Cell Culture
Cell Line
Cell Proliferation - drug effects
Demethylation
Dibutyl Phthalate - toxicity
DNA (Cytosine-5-)-Methyltransferases - genetics
DNA (Cytosine-5-)-Methyltransferases - metabolism
DNA damage
DNA Damage - drug effects
DNA Demethylation
DNA methylation
DNA Methyltransferase 3B
Flagella
Flagella - genetics
Flagella - metabolism
Germ cells
Immunology
Life Sciences
Male
Mice
Mice, Inbred C57BL
MicroRNAs - genetics
MicroRNAs - metabolism
n-Butyl phthalate
Promoter Regions, Genetic
Proto-Oncogene Proteins c-akt - antagonists & inhibitors
Proto-Oncogene Proteins c-akt - genetics
Proto-Oncogene Proteins c-akt - metabolism
PTEN Phosphohydrolase - chemistry
PTEN Phosphohydrolase - genetics
PTEN Phosphohydrolase - metabolism
PTEN protein
Reproductive system
Signal Transduction - drug effects
Sperm
Sperm Motility - drug effects
Sperm Motility - genetics
Spermatozoa - drug effects
Spermatozoa - metabolism
Testis - cytology
Testis - drug effects
Testis - metabolism
Toxicity
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Title Di-n-butyl phthalate epigenetically induces reproductive toxicity via the PTEN/AKT pathway
URI https://link.springer.com/article/10.1038/s41419-019-1547-8
https://www.ncbi.nlm.nih.gov/pubmed/30952838
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Volume 10
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