Downregulation of DJ-1 Fails to Protect Mitochondrial Complex I Subunit NDUFS3 in the Testes and Contributes to the Asthenozoospermia
Asthenozoospermia (AS), an important cause of male infertility, is characterized by reduced sperm motility. Among the aetiologies of AS, inflammation seems to be the main cause. DJ-1, a conserved protein product of the PARK7 gene, is associated with male infertility and plays a role in oxidative str...
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| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2018-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2018/6136075 |
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| author | Yupeng Wang Yi Sun Xin Zhao Renpei Yuan Hui Jiang Xiaoping Pu |
| author_facet | Yupeng Wang Yi Sun Xin Zhao Renpei Yuan Hui Jiang Xiaoping Pu |
| author_sort | Yupeng Wang |
| collection | DOAJ |
| description | Asthenozoospermia (AS), an important cause of male infertility, is characterized by reduced sperm motility. Among the aetiologies of AS, inflammation seems to be the main cause. DJ-1, a conserved protein product of the PARK7 gene, is associated with male infertility and plays a role in oxidative stress and inflammation. Although our previous studies showed that a reduction in DJ-1 was accompanied by mitochondrial dysfunction in the sperm of patients with AS, the specific mechanism underlying this association remained unclear. In this study, we found that compared to the patients without AS, the expression of mitochondrial protein nicotinamide adenine dinucleotide dehydrogenase (ubiquinone) Fe-S protein 3 (NDUFS3) was also significantly decreased in the sperm of patients with AS. Similarly, decreased expression of DJ-1 and NDUFS3 and reduced mitochondria complex I activity were evident in a rat model of AS. Moreover, we showed that the interaction between DJ-1 and NDUFS3 in rat testes was weakened by ORN treatment. These results suggest that the impaired mitochondrial activity could be due to the broken interaction between DJ-1 and NDUFS3 and that downregulation of DJ-1 in sperm and testes contributes to AS pathogenesis. |
| format | Article |
| id | doaj-art-ec8b3a38cb814f21882ff0d91ffed44b |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2018-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-ec8b3a38cb814f21882ff0d91ffed44b2025-02-03T01:32:45ZengWileyMediators of Inflammation0962-93511466-18612018-01-01201810.1155/2018/61360756136075Downregulation of DJ-1 Fails to Protect Mitochondrial Complex I Subunit NDUFS3 in the Testes and Contributes to the AsthenozoospermiaYupeng Wang0Yi Sun1Xin Zhao2Renpei Yuan3Hui Jiang4Xiaoping Pu5National Key Research Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, ChinaNational Key Research Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, ChinaNational Key Research Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, ChinaDepartment of Urology, Peking University Third Hospital, Beijing 100191, ChinaDepartment of Urology, Peking University Third Hospital, Beijing 100191, ChinaNational Key Research Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, ChinaAsthenozoospermia (AS), an important cause of male infertility, is characterized by reduced sperm motility. Among the aetiologies of AS, inflammation seems to be the main cause. DJ-1, a conserved protein product of the PARK7 gene, is associated with male infertility and plays a role in oxidative stress and inflammation. Although our previous studies showed that a reduction in DJ-1 was accompanied by mitochondrial dysfunction in the sperm of patients with AS, the specific mechanism underlying this association remained unclear. In this study, we found that compared to the patients without AS, the expression of mitochondrial protein nicotinamide adenine dinucleotide dehydrogenase (ubiquinone) Fe-S protein 3 (NDUFS3) was also significantly decreased in the sperm of patients with AS. Similarly, decreased expression of DJ-1 and NDUFS3 and reduced mitochondria complex I activity were evident in a rat model of AS. Moreover, we showed that the interaction between DJ-1 and NDUFS3 in rat testes was weakened by ORN treatment. These results suggest that the impaired mitochondrial activity could be due to the broken interaction between DJ-1 and NDUFS3 and that downregulation of DJ-1 in sperm and testes contributes to AS pathogenesis.http://dx.doi.org/10.1155/2018/6136075 |
| spellingShingle | Yupeng Wang Yi Sun Xin Zhao Renpei Yuan Hui Jiang Xiaoping Pu Downregulation of DJ-1 Fails to Protect Mitochondrial Complex I Subunit NDUFS3 in the Testes and Contributes to the Asthenozoospermia Mediators of Inflammation |
| title | Downregulation of DJ-1 Fails to Protect Mitochondrial Complex I Subunit NDUFS3 in the Testes and Contributes to the Asthenozoospermia |
| title_full | Downregulation of DJ-1 Fails to Protect Mitochondrial Complex I Subunit NDUFS3 in the Testes and Contributes to the Asthenozoospermia |
| title_fullStr | Downregulation of DJ-1 Fails to Protect Mitochondrial Complex I Subunit NDUFS3 in the Testes and Contributes to the Asthenozoospermia |
| title_full_unstemmed | Downregulation of DJ-1 Fails to Protect Mitochondrial Complex I Subunit NDUFS3 in the Testes and Contributes to the Asthenozoospermia |
| title_short | Downregulation of DJ-1 Fails to Protect Mitochondrial Complex I Subunit NDUFS3 in the Testes and Contributes to the Asthenozoospermia |
| title_sort | downregulation of dj 1 fails to protect mitochondrial complex i subunit ndufs3 in the testes and contributes to the asthenozoospermia |
| url | http://dx.doi.org/10.1155/2018/6136075 |
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