Abstract
Udgivelsesdato: August
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | Journal of Endocrinology |
| Vol/bind | 194 |
| Udgave nummer | 2 |
| Sider (fra-til) | 417-427 |
| Antal sider | 10 |
| ISSN | 0022-0795 |
| DOI | |
| Status | Udgivet - 2007 |
| Udgivet eksternt | Ja |
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I: Journal of Endocrinology, Bind 194, Nr. 2, 2007, s. 417-427.
Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
}
TY - JOUR
T1 - Cortisol regulation of ion transporter mRNA in Atlantic salmon gill and the effect of salinity on the signaling pathway
AU - Kiilerich, Pia
AU - Kristiansen, Karsten
AU - Madsen, Steffen S
PY - 2007
Y1 - 2007
N2 - Based on real-time RT-PCR, analysis of transcripts of selected ion-regulatory proteins (Na(+), K(+)-ATPase alpha1a and alpha1b subunit, Na(+), K(+), 2Cl(-) cotransporter, cystic fibrosis transmembrane conductance regulator (CFTR), and H(+)-ATPase B-subunit), the regulatory role of cortisol and the associated receptor signaling pathway (glucocorticoid (GR) versus mineralocorticoid (MR)) of cortisol was investigated in the salmon gill. Using a gill organ culture technique, the effect of cortisol with and without addition of specific hormone receptor antagonists (RU486 and spironolactone) was analyzed in gills from freshwater (FW) and seawater (SW) acclimated fish. The effect of cortisol was highly dependent on acclimation to salinity. In FW, cortisol stimulated the transcript levels of CFTR-I and Na(+), K(+)-ATPase alpha1a and alpha1b. Addition of RU486 totally abolished the cortisol effects on CFTR-I and Na(+), K(+)-ATPase alpha1b, suggesting that signaling was mediated via GR. Interestingly, both spironolactone and RU486 were able to inhibit the cortisol effect on Na(+), K(+)-ATPase alpha1a indicating a role for both MR and GR in regulation of this target gene. In SW, cortisol increased the transcript levels of CFTR-I, CFTR-II, Na(+), K(+)-ATPase alpha1a and alpha1b, and NKCC. Interestingly, the effect of cortisol on CFTR-I and Na(+), K(+)-ATPase alpha1a was mediated through GR and MR respectively, while both GR and MR signaling were required in the regulation of CFTR-II and Na(+), K(+)-ATPase alpha1b. In FW gills, GR1 and MR transcript levels were not significantly affected by cortisol. In SW gills, GR1 and MR transcripts were downregulated by cortisol; GR1 was regulated via the MR and MR regulation was mediated via GR.
AB - Based on real-time RT-PCR, analysis of transcripts of selected ion-regulatory proteins (Na(+), K(+)-ATPase alpha1a and alpha1b subunit, Na(+), K(+), 2Cl(-) cotransporter, cystic fibrosis transmembrane conductance regulator (CFTR), and H(+)-ATPase B-subunit), the regulatory role of cortisol and the associated receptor signaling pathway (glucocorticoid (GR) versus mineralocorticoid (MR)) of cortisol was investigated in the salmon gill. Using a gill organ culture technique, the effect of cortisol with and without addition of specific hormone receptor antagonists (RU486 and spironolactone) was analyzed in gills from freshwater (FW) and seawater (SW) acclimated fish. The effect of cortisol was highly dependent on acclimation to salinity. In FW, cortisol stimulated the transcript levels of CFTR-I and Na(+), K(+)-ATPase alpha1a and alpha1b. Addition of RU486 totally abolished the cortisol effects on CFTR-I and Na(+), K(+)-ATPase alpha1b, suggesting that signaling was mediated via GR. Interestingly, both spironolactone and RU486 were able to inhibit the cortisol effect on Na(+), K(+)-ATPase alpha1a indicating a role for both MR and GR in regulation of this target gene. In SW, cortisol increased the transcript levels of CFTR-I, CFTR-II, Na(+), K(+)-ATPase alpha1a and alpha1b, and NKCC. Interestingly, the effect of cortisol on CFTR-I and Na(+), K(+)-ATPase alpha1a was mediated through GR and MR respectively, while both GR and MR signaling were required in the regulation of CFTR-II and Na(+), K(+)-ATPase alpha1b. In FW gills, GR1 and MR transcript levels were not significantly affected by cortisol. In SW gills, GR1 and MR transcripts were downregulated by cortisol; GR1 was regulated via the MR and MR regulation was mediated via GR.
U2 - 10.1677/JOE-07-0185
DO - 10.1677/JOE-07-0185
M3 - Journal article
C2 - 17641289
SN - 0022-0795
VL - 194
SP - 417
EP - 427
JO - Journal of Endocrinology
JF - Journal of Endocrinology
IS - 2
ER -