Distinct hormonal regulation of Na+,K+-atpase genes in the gill of Atlantic salmon (Salmo salar L.)

It has recently become evident that maintenance of ionic homoeostasis in euryhaline salmonids involves a reciprocal shift in expression of two isoforms of the gill Na + ,K + -atpase α-subunit when the surrounding salinity changes. The present study investigated the regulation of this shift between t...

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Published in:Journal of Endocrinology
Main Authors: Tipsmark, Christian K, Madsen, Steffen S
Format: Article in Journal/Newspaper
Language:unknown
Published: Bioscientifica 2009
Subjects:
Online Access:http://dx.doi.org/10.1677/joe-09-0281
https://joe.bioscientifica.com/view/journals/joe/203/2/301.xml
https://joe.bioscientifica.com/downloadpdf/journals/joe/203/2/301.xml
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spelling crbioscientif:10.1677/joe-09-0281 2024-06-23T07:51:24+00:00 Distinct hormonal regulation of Na+,K+-atpase genes in the gill of Atlantic salmon (Salmo salar L.) Tipsmark, Christian K Madsen, Steffen S 2009 http://dx.doi.org/10.1677/joe-09-0281 https://joe.bioscientifica.com/view/journals/joe/203/2/301.xml https://joe.bioscientifica.com/downloadpdf/journals/joe/203/2/301.xml unknown Bioscientifica Journal of Endocrinology volume 203, issue 2, page 301-310 ISSN 0022-0795 1479-6805 journal-article 2009 crbioscientif https://doi.org/10.1677/joe-09-0281 2024-05-30T08:13:39Z It has recently become evident that maintenance of ionic homoeostasis in euryhaline salmonids involves a reciprocal shift in expression of two isoforms of the gill Na + ,K + -atpase α-subunit when the surrounding salinity changes. The present study investigated the regulation of this shift between the α1a (freshwater (FW) isoform) and the α1b (seawater (SW) isoform) by cortisol, Gh, prolactin (Prl) and Igf 1. Injection with cortisol into FW salmon increased α1a expression, while Gh had no effect. Conversely, both cortisol and Gh stimulated α1b expression, and a significant synergy was observed. igf1 expression was increased by Gh in both gill and liver, and inhibited by cortisol in the liver. Gill igf1 and gh receptor expression increased in response to cortisol. Injection with Prl into SW salmon compromised their hypo-osmoregulatory performance, selectively reduced the expression of the α1b isoform and decreased enzymatic Na + ,K + -atpase activity in the gill. Cortisol and Prl reduced gill and liver igf1 expression, and both hormones stimulated gill igf1 receptor expression. In a short-term experiment with incubation of FW gill cell suspensions, cortisol stimulated α1a and α1b expression, while Igf1 stimulated only α1b . The data elaborate our understanding of Prl and Gh as being antagonists in the control of gill ion regulation, and support a dual role for Gh involving endocrine and paracrine Igf1 action. Gh and Prl may be the decisive stimuli that direct cortisol-aided mitochondrion-rich cell development into either secretory or absorptive types. Article in Journal/Newspaper Atlantic salmon Salmo salar Bioscientifica Journal of Endocrinology 203 2 301 310
institution Open Polar
collection Bioscientifica
op_collection_id crbioscientif
language unknown
description It has recently become evident that maintenance of ionic homoeostasis in euryhaline salmonids involves a reciprocal shift in expression of two isoforms of the gill Na + ,K + -atpase α-subunit when the surrounding salinity changes. The present study investigated the regulation of this shift between the α1a (freshwater (FW) isoform) and the α1b (seawater (SW) isoform) by cortisol, Gh, prolactin (Prl) and Igf 1. Injection with cortisol into FW salmon increased α1a expression, while Gh had no effect. Conversely, both cortisol and Gh stimulated α1b expression, and a significant synergy was observed. igf1 expression was increased by Gh in both gill and liver, and inhibited by cortisol in the liver. Gill igf1 and gh receptor expression increased in response to cortisol. Injection with Prl into SW salmon compromised their hypo-osmoregulatory performance, selectively reduced the expression of the α1b isoform and decreased enzymatic Na + ,K + -atpase activity in the gill. Cortisol and Prl reduced gill and liver igf1 expression, and both hormones stimulated gill igf1 receptor expression. In a short-term experiment with incubation of FW gill cell suspensions, cortisol stimulated α1a and α1b expression, while Igf1 stimulated only α1b . The data elaborate our understanding of Prl and Gh as being antagonists in the control of gill ion regulation, and support a dual role for Gh involving endocrine and paracrine Igf1 action. Gh and Prl may be the decisive stimuli that direct cortisol-aided mitochondrion-rich cell development into either secretory or absorptive types.
format Article in Journal/Newspaper
author Tipsmark, Christian K
Madsen, Steffen S
spellingShingle Tipsmark, Christian K
Madsen, Steffen S
Distinct hormonal regulation of Na+,K+-atpase genes in the gill of Atlantic salmon (Salmo salar L.)
author_facet Tipsmark, Christian K
Madsen, Steffen S
author_sort Tipsmark, Christian K
title Distinct hormonal regulation of Na+,K+-atpase genes in the gill of Atlantic salmon (Salmo salar L.)
title_short Distinct hormonal regulation of Na+,K+-atpase genes in the gill of Atlantic salmon (Salmo salar L.)
title_full Distinct hormonal regulation of Na+,K+-atpase genes in the gill of Atlantic salmon (Salmo salar L.)
title_fullStr Distinct hormonal regulation of Na+,K+-atpase genes in the gill of Atlantic salmon (Salmo salar L.)
title_full_unstemmed Distinct hormonal regulation of Na+,K+-atpase genes in the gill of Atlantic salmon (Salmo salar L.)
title_sort distinct hormonal regulation of na+,k+-atpase genes in the gill of atlantic salmon (salmo salar l.)
publisher Bioscientifica
publishDate 2009
url http://dx.doi.org/10.1677/joe-09-0281
https://joe.bioscientifica.com/view/journals/joe/203/2/301.xml
https://joe.bioscientifica.com/downloadpdf/journals/joe/203/2/301.xml
genre Atlantic salmon
Salmo salar
genre_facet Atlantic salmon
Salmo salar
op_source Journal of Endocrinology
volume 203, issue 2, page 301-310
ISSN 0022-0795 1479-6805
op_doi https://doi.org/10.1677/joe-09-0281
container_title Journal of Endocrinology
container_volume 203
container_issue 2
container_start_page 301
op_container_end_page 310
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