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Comparative RNA-sequencing analysis of the prostate in a mouse model of benign prostatic hyperplasia with bladder outlet obstruction

In ageing men, benign prostatic hyperplasia (BPH) is a chronic disease that leads to progressive lower urinary tract symptoms (LUTS) caused by obstruction of the bladder outlet (BOO). Patients with LUTS (such as increased frequency and urgency of urination) and complications of BOO (such as hydronep...

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Autores principales: Tang, Xiaohu, Liu, Zhiyan, Ren, Jingwen, Cao, Ying, Xia, Shujie, Sun, Zhaolin, Luo, Guangheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10628026/
https://www.ncbi.nlm.nih.gov/pubmed/36920576
http://dx.doi.org/10.1007/s11010-023-04695-2
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author Tang, Xiaohu
Liu, Zhiyan
Ren, Jingwen
Cao, Ying
Xia, Shujie
Sun, Zhaolin
Luo, Guangheng
author_facet Tang, Xiaohu
Liu, Zhiyan
Ren, Jingwen
Cao, Ying
Xia, Shujie
Sun, Zhaolin
Luo, Guangheng
author_sort Tang, Xiaohu
collection PubMed
description In ageing men, benign prostatic hyperplasia (BPH) is a chronic disease that leads to progressive lower urinary tract symptoms (LUTS) caused by obstruction of the bladder outlet (BOO). Patients with LUTS (such as increased frequency and urgency of urination) and complications of BOO (such as hydronephrosis and bladder stones) are at risk of serious health problems. BPH causes a rapidly rising burden of LUTS far exceeding that of other urological conditions. Treatment outcomes are unsatisfactory for BPH largely due to the lacking of fully understanding of the pathogenesis. Hormonal imbalances related to androgen and oestrogen can cause BPH, but the exact mechanism is still unknown, even the animal model is not fully understood. Additionally, there are no large-scale data to explain this mechanism. A BPH mouse model was established using mixed slow-release pellets of testosterone (T) and estradiol (E2), and we measured gene expression in mouse prostate tissue using RNA-seq, verified the results using qRT‒PCR, and used bioinformatics methods to analyse the differentially expressed genes (DEGs). SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s11010-023-04695-2.
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spelling pubmed-106280262023-11-08 Comparative RNA-sequencing analysis of the prostate in a mouse model of benign prostatic hyperplasia with bladder outlet obstruction Tang, Xiaohu Liu, Zhiyan Ren, Jingwen Cao, Ying Xia, Shujie Sun, Zhaolin Luo, Guangheng Mol Cell Biochem Article In ageing men, benign prostatic hyperplasia (BPH) is a chronic disease that leads to progressive lower urinary tract symptoms (LUTS) caused by obstruction of the bladder outlet (BOO). Patients with LUTS (such as increased frequency and urgency of urination) and complications of BOO (such as hydronephrosis and bladder stones) are at risk of serious health problems. BPH causes a rapidly rising burden of LUTS far exceeding that of other urological conditions. Treatment outcomes are unsatisfactory for BPH largely due to the lacking of fully understanding of the pathogenesis. Hormonal imbalances related to androgen and oestrogen can cause BPH, but the exact mechanism is still unknown, even the animal model is not fully understood. Additionally, there are no large-scale data to explain this mechanism. A BPH mouse model was established using mixed slow-release pellets of testosterone (T) and estradiol (E2), and we measured gene expression in mouse prostate tissue using RNA-seq, verified the results using qRT‒PCR, and used bioinformatics methods to analyse the differentially expressed genes (DEGs). SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s11010-023-04695-2. Springer US 2023-03-15 2023 /pmc/articles/PMC10628026/ /pubmed/36920576 http://dx.doi.org/10.1007/s11010-023-04695-2 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/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/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Tang, Xiaohu
Liu, Zhiyan
Ren, Jingwen
Cao, Ying
Xia, Shujie
Sun, Zhaolin
Luo, Guangheng
Comparative RNA-sequencing analysis of the prostate in a mouse model of benign prostatic hyperplasia with bladder outlet obstruction
title Comparative RNA-sequencing analysis of the prostate in a mouse model of benign prostatic hyperplasia with bladder outlet obstruction
title_full Comparative RNA-sequencing analysis of the prostate in a mouse model of benign prostatic hyperplasia with bladder outlet obstruction
title_fullStr Comparative RNA-sequencing analysis of the prostate in a mouse model of benign prostatic hyperplasia with bladder outlet obstruction
title_full_unstemmed Comparative RNA-sequencing analysis of the prostate in a mouse model of benign prostatic hyperplasia with bladder outlet obstruction
title_short Comparative RNA-sequencing analysis of the prostate in a mouse model of benign prostatic hyperplasia with bladder outlet obstruction
title_sort comparative rna-sequencing analysis of the prostate in a mouse model of benign prostatic hyperplasia with bladder outlet obstruction
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10628026/
https://www.ncbi.nlm.nih.gov/pubmed/36920576
http://dx.doi.org/10.1007/s11010-023-04695-2
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