Cargando…
Enhanced Hypoxia-Associated Genes in Impaired Contractility From Bladder Outlet Obstruction
BACKGROUND: Hypoxia damages the bladder wall and contributes to the initiation of bladder dysfunction. The change of hypoxia is not well known in impaired bladder contractility caused by long-term bladder outlet obstruction (BOO). We aimed to find out whether hypoxia of bladder tissue is present and...
Autores principales: | , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Academy of Medical Sciences
2022
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8921211/ https://www.ncbi.nlm.nih.gov/pubmed/35289143 http://dx.doi.org/10.3346/jkms.2022.37.e84 |
_version_ | 1784669287852539904 |
---|---|
author | Kim, Jae Heon Yang, Hee Jo Lee, Hong J. Song, Yun Seob |
author_facet | Kim, Jae Heon Yang, Hee Jo Lee, Hong J. Song, Yun Seob |
author_sort | Kim, Jae Heon |
collection | PubMed |
description | BACKGROUND: Hypoxia damages the bladder wall and contributes to the initiation of bladder dysfunction. The change of hypoxia is not well known in impaired bladder contractility caused by long-term bladder outlet obstruction (BOO). We aimed to find out whether hypoxia of bladder tissue is present and what signaling mechanisms are involved in the decompensated bladder in BOO. METHODS: Twenty 6-week-old female Sprague-Dawley rats were divided into 2 groups, 10 rats each: group 1, sham operation; group 2, BOO for 8 weeks. Eight weeks after the onset of BOO, we did cystometric evaluation and processed polymerase chain reaction (PCR) array for hypoxia pathway using bladder tissues. The PCR array consists of 84 genes known to be involved in the hypoxic response, cell differentiation, and metabolism. We did quantitative PCR (qPCR) and immunohistochemical staining of bladder tissue for hypoxia. RESULTS: Eight genes were at least 2-fold upregulated and 3 genes were at least 2-fold downregulated in BOO group, compared with the sham operation group. The up-regulated genes (fold change) belonging to the hypoxia-inducible factor (HIF) 1 interactor included Cdkn2a (11.0), and the down-regulated genes belonging to HIF and co-transcription factors included Hif3a (−39.6) and Per1 (−5.1) by BOO. Genes influenced each other by means of TGFβ1, TNF, and TP53. CONCLUSION: Hypoxia genes were increased in impaired contractility because of long-term BOO. The gene expression profiles could explain the molecular mechanisms of hypoxia in impaired contractility because of long-term BOO. |
format | Online Article Text |
id | pubmed-8921211 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | The Korean Academy of Medical Sciences |
record_format | MEDLINE/PubMed |
spelling | pubmed-89212112022-03-22 Enhanced Hypoxia-Associated Genes in Impaired Contractility From Bladder Outlet Obstruction Kim, Jae Heon Yang, Hee Jo Lee, Hong J. Song, Yun Seob J Korean Med Sci Original Article BACKGROUND: Hypoxia damages the bladder wall and contributes to the initiation of bladder dysfunction. The change of hypoxia is not well known in impaired bladder contractility caused by long-term bladder outlet obstruction (BOO). We aimed to find out whether hypoxia of bladder tissue is present and what signaling mechanisms are involved in the decompensated bladder in BOO. METHODS: Twenty 6-week-old female Sprague-Dawley rats were divided into 2 groups, 10 rats each: group 1, sham operation; group 2, BOO for 8 weeks. Eight weeks after the onset of BOO, we did cystometric evaluation and processed polymerase chain reaction (PCR) array for hypoxia pathway using bladder tissues. The PCR array consists of 84 genes known to be involved in the hypoxic response, cell differentiation, and metabolism. We did quantitative PCR (qPCR) and immunohistochemical staining of bladder tissue for hypoxia. RESULTS: Eight genes were at least 2-fold upregulated and 3 genes were at least 2-fold downregulated in BOO group, compared with the sham operation group. The up-regulated genes (fold change) belonging to the hypoxia-inducible factor (HIF) 1 interactor included Cdkn2a (11.0), and the down-regulated genes belonging to HIF and co-transcription factors included Hif3a (−39.6) and Per1 (−5.1) by BOO. Genes influenced each other by means of TGFβ1, TNF, and TP53. CONCLUSION: Hypoxia genes were increased in impaired contractility because of long-term BOO. The gene expression profiles could explain the molecular mechanisms of hypoxia in impaired contractility because of long-term BOO. The Korean Academy of Medical Sciences 2022-03-08 /pmc/articles/PMC8921211/ /pubmed/35289143 http://dx.doi.org/10.3346/jkms.2022.37.e84 Text en © 2022 The Korean Academy of Medical Sciences. https://creativecommons.org/licenses/by-nc/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Kim, Jae Heon Yang, Hee Jo Lee, Hong J. Song, Yun Seob Enhanced Hypoxia-Associated Genes in Impaired Contractility From Bladder Outlet Obstruction |
title | Enhanced Hypoxia-Associated Genes in Impaired Contractility From Bladder Outlet Obstruction |
title_full | Enhanced Hypoxia-Associated Genes in Impaired Contractility From Bladder Outlet Obstruction |
title_fullStr | Enhanced Hypoxia-Associated Genes in Impaired Contractility From Bladder Outlet Obstruction |
title_full_unstemmed | Enhanced Hypoxia-Associated Genes in Impaired Contractility From Bladder Outlet Obstruction |
title_short | Enhanced Hypoxia-Associated Genes in Impaired Contractility From Bladder Outlet Obstruction |
title_sort | enhanced hypoxia-associated genes in impaired contractility from bladder outlet obstruction |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8921211/ https://www.ncbi.nlm.nih.gov/pubmed/35289143 http://dx.doi.org/10.3346/jkms.2022.37.e84 |
work_keys_str_mv | AT kimjaeheon enhancedhypoxiaassociatedgenesinimpairedcontractilityfrombladderoutletobstruction AT yangheejo enhancedhypoxiaassociatedgenesinimpairedcontractilityfrombladderoutletobstruction AT leehongj enhancedhypoxiaassociatedgenesinimpairedcontractilityfrombladderoutletobstruction AT songyunseob enhancedhypoxiaassociatedgenesinimpairedcontractilityfrombladderoutletobstruction |