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Eel osmotic stress transcriptional factor 1 (Ostf1) is highly expressed in gill mitochondria-rich cells, where ERK phosphorylated
BACKGROUND: Osmotic stress transcriptional factor 1 (Ostf1) was firstly identified in tilapia in 2005. Then numerous studies have investigated its regulation and expression profile in fish gill tissues in related to osmoregulation. Generally, hyperosmotic stress induced ostf1 mRNA expression level,...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3315740/ https://www.ncbi.nlm.nih.gov/pubmed/22405401 http://dx.doi.org/10.1186/1742-9994-9-3 |
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author | Tse, William KF Chow, Sheung C Wong, Chris KC |
author_facet | Tse, William KF Chow, Sheung C Wong, Chris KC |
author_sort | Tse, William KF |
collection | PubMed |
description | BACKGROUND: Osmotic stress transcriptional factor 1 (Ostf1) was firstly identified in tilapia in 2005. Then numerous studies have investigated its regulation and expression profile in fish gill tissues in related to osmoregulation. Generally, hyperosmotic stress induced ostf1 mRNA expression level, however there is no report studying the cellular localization of Ostf1 expression in any osmoregulatory tissue. In this study immunohistochemical (IHC) approach was used to study the cellular localization of Ostf1 in gill cells of Japanese eels. FINDINGS: Ostf1 protein was found to be localized in branchial mitochondria-rich/chloride cell (MRC/CC) as revealed by Naα5 and CFTR co-localization. The protein was detectable at day 3 after fresh water to seawater transfer and was mainly localized in MRCs. Moreover, elevated levels of extracellular signal regulated kinase (ERK) phosphorylation was observed at day 3 of the transfer and was co-localized with MRCs. CONCLUSIONS: Our data identified Ostf1 expression in gill MRCs. The observation supports the role of Ostf1 in osmosensing and/or osmoregulation in fish gills, particularly its functional relationship with MRCs. The observation of the co-expression of pERK and Ostf1 in MRCs suggests a cross-talk mechanism between the mitogen-activated protein kinases (MAPKs) and Ostf1 in response to hyperosmotic challenge. To summarize, this report has addressed the cellular localization of Ostf1 and provides evidence to illustrate the involvement of Ostf1 and ERK on osmosensing and osmoregulatory function of gill MRCs. |
format | Online Article Text |
id | pubmed-3315740 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-33157402012-03-31 Eel osmotic stress transcriptional factor 1 (Ostf1) is highly expressed in gill mitochondria-rich cells, where ERK phosphorylated Tse, William KF Chow, Sheung C Wong, Chris KC Front Zool Short Report BACKGROUND: Osmotic stress transcriptional factor 1 (Ostf1) was firstly identified in tilapia in 2005. Then numerous studies have investigated its regulation and expression profile in fish gill tissues in related to osmoregulation. Generally, hyperosmotic stress induced ostf1 mRNA expression level, however there is no report studying the cellular localization of Ostf1 expression in any osmoregulatory tissue. In this study immunohistochemical (IHC) approach was used to study the cellular localization of Ostf1 in gill cells of Japanese eels. FINDINGS: Ostf1 protein was found to be localized in branchial mitochondria-rich/chloride cell (MRC/CC) as revealed by Naα5 and CFTR co-localization. The protein was detectable at day 3 after fresh water to seawater transfer and was mainly localized in MRCs. Moreover, elevated levels of extracellular signal regulated kinase (ERK) phosphorylation was observed at day 3 of the transfer and was co-localized with MRCs. CONCLUSIONS: Our data identified Ostf1 expression in gill MRCs. The observation supports the role of Ostf1 in osmosensing and/or osmoregulation in fish gills, particularly its functional relationship with MRCs. The observation of the co-expression of pERK and Ostf1 in MRCs suggests a cross-talk mechanism between the mitogen-activated protein kinases (MAPKs) and Ostf1 in response to hyperosmotic challenge. To summarize, this report has addressed the cellular localization of Ostf1 and provides evidence to illustrate the involvement of Ostf1 and ERK on osmosensing and osmoregulatory function of gill MRCs. BioMed Central 2012-03-10 /pmc/articles/PMC3315740/ /pubmed/22405401 http://dx.doi.org/10.1186/1742-9994-9-3 Text en Copyright ©2012 Tse et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Short Report Tse, William KF Chow, Sheung C Wong, Chris KC Eel osmotic stress transcriptional factor 1 (Ostf1) is highly expressed in gill mitochondria-rich cells, where ERK phosphorylated |
title | Eel osmotic stress transcriptional factor 1 (Ostf1) is highly expressed in gill mitochondria-rich cells, where ERK phosphorylated |
title_full | Eel osmotic stress transcriptional factor 1 (Ostf1) is highly expressed in gill mitochondria-rich cells, where ERK phosphorylated |
title_fullStr | Eel osmotic stress transcriptional factor 1 (Ostf1) is highly expressed in gill mitochondria-rich cells, where ERK phosphorylated |
title_full_unstemmed | Eel osmotic stress transcriptional factor 1 (Ostf1) is highly expressed in gill mitochondria-rich cells, where ERK phosphorylated |
title_short | Eel osmotic stress transcriptional factor 1 (Ostf1) is highly expressed in gill mitochondria-rich cells, where ERK phosphorylated |
title_sort | eel osmotic stress transcriptional factor 1 (ostf1) is highly expressed in gill mitochondria-rich cells, where erk phosphorylated |
topic | Short Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3315740/ https://www.ncbi.nlm.nih.gov/pubmed/22405401 http://dx.doi.org/10.1186/1742-9994-9-3 |
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