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Label-free proteomics uncovers SMC1A expression is Down-regulated in AUB-E
BACKGROUND: While heavy menstrual bleeding (HMB) is a prevalent symptom among women with abnormal uterine bleeding caused by endometrial disorder (AUB-E) seeking gynecologic care, the primary endometrial disorder remains poorly understood. METHODS: Five human endometrial samples from women with AUB-...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7923474/ https://www.ncbi.nlm.nih.gov/pubmed/33653363 http://dx.doi.org/10.1186/s12958-021-00713-4 |
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author | Jia, Yingxian Luo, Jie Lan, Yibing Li, Chunming Ma, Linjuan Zhu, Xiaoming Ruan, Fei Zhou, Jianhong |
author_facet | Jia, Yingxian Luo, Jie Lan, Yibing Li, Chunming Ma, Linjuan Zhu, Xiaoming Ruan, Fei Zhou, Jianhong |
author_sort | Jia, Yingxian |
collection | PubMed |
description | BACKGROUND: While heavy menstrual bleeding (HMB) is a prevalent symptom among women with abnormal uterine bleeding caused by endometrial disorder (AUB-E) seeking gynecologic care, the primary endometrial disorder remains poorly understood. METHODS: Five human endometrial samples from women with AUB-E and the age-matched healthy women were selected, respectively. Proteins from the samples were analyzed by a linear ion trap (LTQ)-Orbitrap Elite mass spectrometer based label-free proteomic approach. The purpose protein was validated by western blot and immunohistochemistry staining. RESULTS: A total of 2353 protein groups were quantified under highly stringent criteria with a false discovery rate of < 1% for protein groups, and 291 differentially expressed proteins were significantly changed between the two groups. The results showed that the down-regulation of structural maintenance of chromosomes protein 1A (SMC1A) in AUB-E patients. Next, this change in the glandular epithelial cells was validated by immunohistochemistry. CONCLUSION: The results indicated a novel mechanism for the cause of AUB-E, as down-expression SMC1A potentially regulated the cell cycle progression in endometrial glandular epithelium further led to bleeding. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12958-021-00713-4. |
format | Online Article Text |
id | pubmed-7923474 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-79234742021-03-02 Label-free proteomics uncovers SMC1A expression is Down-regulated in AUB-E Jia, Yingxian Luo, Jie Lan, Yibing Li, Chunming Ma, Linjuan Zhu, Xiaoming Ruan, Fei Zhou, Jianhong Reprod Biol Endocrinol Research BACKGROUND: While heavy menstrual bleeding (HMB) is a prevalent symptom among women with abnormal uterine bleeding caused by endometrial disorder (AUB-E) seeking gynecologic care, the primary endometrial disorder remains poorly understood. METHODS: Five human endometrial samples from women with AUB-E and the age-matched healthy women were selected, respectively. Proteins from the samples were analyzed by a linear ion trap (LTQ)-Orbitrap Elite mass spectrometer based label-free proteomic approach. The purpose protein was validated by western blot and immunohistochemistry staining. RESULTS: A total of 2353 protein groups were quantified under highly stringent criteria with a false discovery rate of < 1% for protein groups, and 291 differentially expressed proteins were significantly changed between the two groups. The results showed that the down-regulation of structural maintenance of chromosomes protein 1A (SMC1A) in AUB-E patients. Next, this change in the glandular epithelial cells was validated by immunohistochemistry. CONCLUSION: The results indicated a novel mechanism for the cause of AUB-E, as down-expression SMC1A potentially regulated the cell cycle progression in endometrial glandular epithelium further led to bleeding. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12958-021-00713-4. BioMed Central 2021-03-02 /pmc/articles/PMC7923474/ /pubmed/33653363 http://dx.doi.org/10.1186/s12958-021-00713-4 Text en © The Author(s) 2021 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Jia, Yingxian Luo, Jie Lan, Yibing Li, Chunming Ma, Linjuan Zhu, Xiaoming Ruan, Fei Zhou, Jianhong Label-free proteomics uncovers SMC1A expression is Down-regulated in AUB-E |
title | Label-free proteomics uncovers SMC1A expression is Down-regulated in AUB-E |
title_full | Label-free proteomics uncovers SMC1A expression is Down-regulated in AUB-E |
title_fullStr | Label-free proteomics uncovers SMC1A expression is Down-regulated in AUB-E |
title_full_unstemmed | Label-free proteomics uncovers SMC1A expression is Down-regulated in AUB-E |
title_short | Label-free proteomics uncovers SMC1A expression is Down-regulated in AUB-E |
title_sort | label-free proteomics uncovers smc1a expression is down-regulated in aub-e |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7923474/ https://www.ncbi.nlm.nih.gov/pubmed/33653363 http://dx.doi.org/10.1186/s12958-021-00713-4 |
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