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The frequency of TP53 R72P and MDM2 309T>G polymorphisms in Iranian infertile men with spermatogenetic failure: A case-control study
BACKGROUND: Tumor protein p53 (TP53) is a tumor suppressor transcriptional regulator protein which plays a critical role in the spermatogenesis. One of the most important regulators of p53 is Murine double minute 2 (MDM2), which acts as a negative regulator of the p53 pathway. Based on the key role...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Research and Clinical Center for Infertility
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6163049/ https://www.ncbi.nlm.nih.gov/pubmed/30288482 |
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author | Ebrahim Abadi, Zeinab Khademi Bami, Maryam Golzadeh, Maryam Kalantar, Seyed Mehdi Sheikhha, Mohammad Hasan |
author_facet | Ebrahim Abadi, Zeinab Khademi Bami, Maryam Golzadeh, Maryam Kalantar, Seyed Mehdi Sheikhha, Mohammad Hasan |
author_sort | Ebrahim Abadi, Zeinab |
collection | PubMed |
description | BACKGROUND: Tumor protein p53 (TP53) is a tumor suppressor transcriptional regulator protein which plays a critical role in the spermatogenesis. One of the most important regulators of p53 is Murine double minute 2 (MDM2), which acts as a negative regulator of the p53 pathway. Based on the key role of p53 and MDM2 in germ cell apoptosis, polymorphisms that cause a change in their function might affect germ cell apoptosis and the risk of male infertility. OBJECTIVE: This study was designed to examine associations of TP53 72 Arg>Pro (rs1042522), and MDM2 309 T>G (rs937283) polymorphisms with spermatogenetic failure in Iranian population. MATERIALS AND METHODS: A case-control study was conducted with 150 nonobstructive azoospermia or severe oligozoospermia and 150 fertile controls. The two polymorphisms, 72 Arg>Pro in TP53 and 309 T>G in MDM2, were genotyped using PCR-RFLP and ARMS-PCR respectively. RESULTS: Our analyses revealed that the allele and genotype frequencies of the TP53 R72P polymorphism were not significantly different between the cases and controls (p=0.41, p=0.40 respectively). Also, no significant differences were found in the allelic (p=0.46) and genotypic (p=0.78) distribution of MDM2 309 T>G polymorphism between patients and controls. CONCLUSION: The results of this study indicate that polymorphisms of TP53 and MDM2 genes are unlikely to contribute to the pathogenesis of male infertility with spermatogenetic failure. |
format | Online Article Text |
id | pubmed-6163049 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Research and Clinical Center for Infertility |
record_format | MEDLINE/PubMed |
spelling | pubmed-61630492018-10-04 The frequency of TP53 R72P and MDM2 309T>G polymorphisms in Iranian infertile men with spermatogenetic failure: A case-control study Ebrahim Abadi, Zeinab Khademi Bami, Maryam Golzadeh, Maryam Kalantar, Seyed Mehdi Sheikhha, Mohammad Hasan Int J Reprod Biomed Original Article BACKGROUND: Tumor protein p53 (TP53) is a tumor suppressor transcriptional regulator protein which plays a critical role in the spermatogenesis. One of the most important regulators of p53 is Murine double minute 2 (MDM2), which acts as a negative regulator of the p53 pathway. Based on the key role of p53 and MDM2 in germ cell apoptosis, polymorphisms that cause a change in their function might affect germ cell apoptosis and the risk of male infertility. OBJECTIVE: This study was designed to examine associations of TP53 72 Arg>Pro (rs1042522), and MDM2 309 T>G (rs937283) polymorphisms with spermatogenetic failure in Iranian population. MATERIALS AND METHODS: A case-control study was conducted with 150 nonobstructive azoospermia or severe oligozoospermia and 150 fertile controls. The two polymorphisms, 72 Arg>Pro in TP53 and 309 T>G in MDM2, were genotyped using PCR-RFLP and ARMS-PCR respectively. RESULTS: Our analyses revealed that the allele and genotype frequencies of the TP53 R72P polymorphism were not significantly different between the cases and controls (p=0.41, p=0.40 respectively). Also, no significant differences were found in the allelic (p=0.46) and genotypic (p=0.78) distribution of MDM2 309 T>G polymorphism between patients and controls. CONCLUSION: The results of this study indicate that polymorphisms of TP53 and MDM2 genes are unlikely to contribute to the pathogenesis of male infertility with spermatogenetic failure. Research and Clinical Center for Infertility 2018-08 /pmc/articles/PMC6163049/ /pubmed/30288482 Text en This is an Open Access article distributed under the terms of the Creative Commons Attribution License, (http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Ebrahim Abadi, Zeinab Khademi Bami, Maryam Golzadeh, Maryam Kalantar, Seyed Mehdi Sheikhha, Mohammad Hasan The frequency of TP53 R72P and MDM2 309T>G polymorphisms in Iranian infertile men with spermatogenetic failure: A case-control study |
title | The frequency of TP53 R72P and MDM2 309T>G polymorphisms in Iranian infertile men with spermatogenetic failure: A case-control study |
title_full | The frequency of TP53 R72P and MDM2 309T>G polymorphisms in Iranian infertile men with spermatogenetic failure: A case-control study |
title_fullStr | The frequency of TP53 R72P and MDM2 309T>G polymorphisms in Iranian infertile men with spermatogenetic failure: A case-control study |
title_full_unstemmed | The frequency of TP53 R72P and MDM2 309T>G polymorphisms in Iranian infertile men with spermatogenetic failure: A case-control study |
title_short | The frequency of TP53 R72P and MDM2 309T>G polymorphisms in Iranian infertile men with spermatogenetic failure: A case-control study |
title_sort | frequency of tp53 r72p and mdm2 309t>g polymorphisms in iranian infertile men with spermatogenetic failure: a case-control study |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6163049/ https://www.ncbi.nlm.nih.gov/pubmed/30288482 |
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