PUBLICATION
Cortisol regulates sodium homeostasis by stimulating the transcription of sodium-chloride transporter (NCC) in zebrafish (Danio rerio)
- Authors
- Lin, C.H., Hu, H.J., Hwang, P.P.
- ID
- ZDB-PUB-151219-8
- Date
- 2016
- Source
- Molecular and Cellular Endocrinology 422: 93-102 (Journal)
- Registered Authors
- Hwang, Pung Pung
- Keywords
- NCC, cortisol, ionocyte, sodium absorption, zebrafish
- MeSH Terms
-
- Animals
- Anti-Inflammatory Agents/pharmacology*
- Embryo, Nonmammalian/drug effects
- Embryo, Nonmammalian/enzymology
- Gene Expression Regulation/drug effects
- Homeostasis
- Hydrocortisone/pharmacology*
- Sodium/metabolism*
- Sodium Chloride Symporters/genetics*
- Zebrafish/embryology*
- Zebrafish/genetics
- Zebrafish Proteins/genetics
- PubMed
- 26678829 Full text @ Mol. Cell. Endocrinol.
Citation
Lin, C.H., Hu, H.J., Hwang, P.P. (2016) Cortisol regulates sodium homeostasis by stimulating the transcription of sodium-chloride transporter (NCC) in zebrafish (Danio rerio). Molecular and Cellular Endocrinology. 422:93-102.
Abstract
In mammals, sodium/hydrogen exchanger (NHE) and sodium-chloride cotransporter (NCC) are expressed in renal tubules, and exhibit functional redundancy and mutual compensation in Na(+) uptake. In teleosts, the gills of the adult and skin of the embryonic stage function as external kidneys, and ionocytes are responsible for ionoregulation in these tissues. NHE- and NCC-expressing ionocytes mutually cooperate to adjust Na(+) uptake, which is analogous to the activity of the mammalian kidney. Cortisol is a hormone that controls Na(+) uptake through regulating NCC expression and activity in mammals; however, cortisol-mediated control of NCC expression is little understood in non-mammalian vertebrates, such as teleosts. It is essential for our understanding of the evolution of such regulation to determine whether cortisol has a conserved effect on NCC in vertebrates. In the present study, we treated zebrafish embryos with low Na(+) medium (LNa, 0.04 mM Na(+)) for 3 d to stimulate the mRNA expression of nhe3b, ncc, and cyp11b1 (a cortisol-synthesis enzyme) and whole body cortisol level. Exogenous cortisol treatment (20 mg/L, 3 d) resulted in an elevation of whole-body Na(+) content, ncc expression, and the density of ncc-expressing cells in zebrafish larvae. In loss-of-function experiments, microinjection of glucocorticoid receptor (gr) morpholino (MO) suppressed sodium content, ncc expression, and the density of ncc-expressing cells, but injection of mr MO had no such effects. In addition, exogenous cortisol treatment and gr MO injection also altered ncc expression and the density of ncc-expressing cells in gcm2 morphant larvae. Taken together, cortisol and GR appear to regulate Na(+) absorption through stimulating ncc expression and the differentiation of ncc-expressing ionocytes, providing new insights into the actions of cortisol on Na(+) uptake.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping