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Cortisol regulation of ion transporter mRNA in Atlantic salmon gill and the effect of salinity on the signaling pathway.
J Endocrinol 2007; 194(2):417-27JE

Abstract

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.

Authors+Show Affiliations

Institute of Biology, University of Southern Denmark, Odense, Campusvej 55, DK-5230 Odense M, Denmark.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17641289

Citation

Kiilerich, Pia, et al. "Cortisol Regulation of Ion Transporter mRNA in Atlantic Salmon Gill and the Effect of Salinity On the Signaling Pathway." The Journal of Endocrinology, vol. 194, no. 2, 2007, pp. 417-27.
Kiilerich P, Kristiansen K, Madsen SS. Cortisol regulation of ion transporter mRNA in Atlantic salmon gill and the effect of salinity on the signaling pathway. J Endocrinol. 2007;194(2):417-27.
Kiilerich, P., Kristiansen, K., & Madsen, S. S. (2007). Cortisol regulation of ion transporter mRNA in Atlantic salmon gill and the effect of salinity on the signaling pathway. The Journal of Endocrinology, 194(2), pp. 417-27.
Kiilerich P, Kristiansen K, Madsen SS. Cortisol Regulation of Ion Transporter mRNA in Atlantic Salmon Gill and the Effect of Salinity On the Signaling Pathway. J Endocrinol. 2007;194(2):417-27. PubMed PMID: 17641289.
* Article titles in AMA citation format should be in sentence-case
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 - 2007/7/21/pubmed PY - 2007/10/27/medline PY - 2007/7/21/entrez SP - 417 EP - 27 JF - The Journal of endocrinology JO - J. Endocrinol. VL - 194 IS - 2 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. SN - 0022-0795 UR - https://www.unboundmedicine.com/medline/citation/17641289/Cortisol_regulation_of_ion_transporter_mRNA_in_Atlantic_salmon_gill_and_the_effect_of_salinity_on_the_signaling_pathway_ L2 - https://joe.bioscientifica.com/doi/10.1677/JOE-07-0185 DB - PRIME DP - Unbound Medicine ER -