Characterization of the zebrafish (Danio rerio) mineralocorticoid receptor

Pippal, Jyotsna B.; Cheung, Ching Mei Irene; Yao, Yizhou; Brennan, Francine E.; Fuller, Peter J.

doi:10.1016/j.mce.2010.09.014

Cited by 84 publications

(92 citation statements)

References 38 publications

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“…Although Kumai et al (2012a) suggested that MR does not play a significant role in the regulation of Na C uptake in zebrafish during chronic exposure to acidic water, in this study we tested the hypothesis that cortisol might interact with MR during acute challenge with acidic or ion-poor water. Treating larvae with 10 mM eplerenone, a recently developed MR inhibitor known to be effective in zebrafish (Pippal et al 2010), did not hinder the capacity of fish to increase Na C uptake during acute exposure to acidic or ion-poor water (data not shown). Thus, the effect of ANG-II on Na C uptake reported in this study is likely to be cortisol-independent.…”

Section: Does Ras Interact With Cortisol In Zebrafish?mentioning

confidence: 91%

Angiotensin-II promotes Na+ uptake in larval zebrafish, Danio rerio, in acidic and ion-poor water

Kumai

Bernier

Perry

2013

Journal of Endocrinology

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The contribution of the renin-angiotensin system (RAS) to Na C uptake was investigated in larval zebrafish (Danio rerio). At 4 days post fertilization (dpf), the level of whole-body angiotensin-II (ANG-II) was significantly increased after 1-or 3-h exposure to acidic (pHZ4.0) or ion-poor water (20-fold dilution of Ottawa tapwater), suggesting rapid activation of the RAS. Long-term (24 h) treatment of 3 dpf larvae with ANG-I or ANG-II significantly increased Na C uptake which was accompanied by an increase in mRNA expression of the NaInduction of Na C uptake by exposure to ANG-I was blocked by simultaneously treating larvae with lisinopril (an angiotensin-converting enzyme inhibitor). Acute (2 h) exposure to acidic water or ion-poor water led to significant increase in Na C uptake which was partially blocked by the ANG-II receptor antagonist, telmisartan. Consistent with these data, translational knockdown of renin prevented the stimulation of Na C uptake following exposure to acidic or ion-poor water. The lack of any effects of pharmacological inhibition (using RU486), or knockdown of glucocorticoid receptors on the stimulation of Na C uptake during acute exposure to acidic or ion-poor environments, indicates that the acute effects of RAS occur independently of cortisol signaling. The results of this study demonstrate that the RAS is involved in Na C homeostasis in larval zebrafish. Key Words" angiotensin-II" cortisol " zebrafish " osmoregulation " ion-poor water " acidic water

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Section: Does Ras Interact With Cortisol In Zebrafish?mentioning

confidence: 91%

Angiotensin-II promotes Na+ uptake in larval zebrafish, Danio rerio, in acidic and ion-poor water

Kumai

Bernier

Perry

2013

Journal of Endocrinology

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“…The EC50 of F is 0.02 nM for cichlid (Greenwood et al 2003, 1).1 nM for trout (Sturm et al 2005, 2).4 nM for carp (Stolte et al 2008) and 0.22 nM for zebrafish (Pippal et al 2011).…”

Section: Ser-843 In Human Mr: Role In Divergence From the Grmentioning

confidence: 99%

“…Aldo first appears in lungfish (Joss et al 1994, Rossier et al 2015, which also secrete F and B. Lungfish are the closest extant forerunners of tetrapods (Woolston 2013). (Rupprecht et al 1993b, Geller 2000 and an agonist for fish MRs (Sturm et al 2005, Pippal et al 2011, Sugimoto et al 2016.…”

Section: Introductionmentioning

confidence: 99%

“…11βHSD2 first appears in Chondrichthyes , Rossier et al 2015, in which 11βHSD2 may regulate access of B to the MR. Although Aldo is not found in ray-finned fish, Aldo is a strong transcriptional activator of fish MR (Greenwood et al 2003, Sturm et al 2005, Stolte et al 2008, Pippal et al 2011, Sugimoto et al 2016. Indeed, the physiological mineralocorticoid in ray-finned fish is not fully understood because several 3-ketosteroids, including F, DOC, B, S and Prog are transcriptional activators of the MR (Greenwood et al 2003, Sturm et al 2005, Stolte et al 2008, Pippal et al 2011, Sugimoto et al 2016, and one or more of these steroids could be a physiological mineralocorticoid.…”

Section: Introductionmentioning

confidence: 99%

“…Thus, during the evolution of the MR in cartilaginous fishes, ray-finned fishes and terrestrial vertebrates, there have been changes in the EC50 of the MR for 3-ketosteroids (Sturm et al 2005, Carroll et al 2008, Pippal et al 2011, Sugimoto et al 2016, as well as the MR's physiological function (Vize & Smith 2004, Hawkins et al 2012, Martinerie et al 2013, Rossier et al 2015, Jaisser & Farman 2016, Mifsud & Reul 2016, Sakamoto et al 2016. It needs to be noted that transcriptional activation by corticosteroids of fish MRs is studied in mammalian cells, which may provide different responses than in assays using homologous fish cells.…”

Section: Introductionmentioning

confidence: 99%

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30 YEARS OF THE MINERALOCORTICOID RECEPTOR: Evolution of the mineralocorticoid receptor: sequence, structure and function

Baker

Katsu

2017

Journal of Endocrinology

119

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The mineralocorticoid receptor (MR) is descended from a corticoid receptor (CR), which has descendants in lamprey and hagfish, cyclostomes (jawless fish), a taxon that evolved at the base of the vertebrate line. A distinct MR and GR first appear in cartilaginous fishes (Chondrichthyes), such as sharks, skates, rays and chimeras. Skate MR has a strong response to corticosteroids that are mineralocorticoids and glucocorticoids in humans. The half-maximal responses (EC50s) for skate MR for the mineralocorticoids aldosterone and 11-deoxycorticosterone are 0.07 nM and 0.03 nM, respectively. EC50s for the glucocorticoids cortisol and corticosterone are 1 nM and 0.09 nM, respectively. The physiological mineralocorticoid in ray-finned fish, which do not synthesize aldosterone, is not fully understood because several 3-ketosteroids, including cortisol, 11-deoxycortisol, corticosterone, 11-deoxycorticosterone and progesterone are transcriptional activators of fish MR. Further divergence of the MR and GR in terrestrial vertebrates, which synthesize aldosterone, led to emergence of aldosterone as a selective ligand for the MR. Here, we combine sequence analysis of the CR and vertebrate MRs and GRs, analysis of crystal structures of human MR and GR and data on transcriptional activation by 3-ketosteroids of wild-type and mutant MRs and GRs to investigate the evolution of selectivity for 3-ketosteroids by the MR in terrestrial vertebrates and ray-finned fish, as well as the basis for binding of some glucocorticoids by human MR and other vertebrate MRs.

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Mineralocorticoid receptor activates postnatal adiposity in zebrafish lacking proopiomelanocortin

Rajeswari,

Faught,

Santos

et al. 2024

Journal Cellular Physiology

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The proopiomelanocortin (Pomc)‐derived peptides, including adrenocorticotropic hormone and α‐melanocyte stimulating hormone (α‐Msh), play both a central and a peripheral role in modulating the stress response. The central role is predominantly associated with nutrient homeostasis, while peripherally they play an important role in the synthesis of glucocorticoids (GCs) in response to stress. Pomc mutations are a major risk factor in the development of early‐onset childhood obesity in humans. This is attributed primarily to their central effects on melanocortin receptor dysfunction leading to hyperphagia and reduced energy expenditure, while the peripheral mechanism contributing to obesity has largely been unexplored. Here, we tested the hypothesis that Pomc mutation‐mediated adrenal insufficiency and the associated changes in GC signaling contribute to postnatal adiposity using zebrafish as a model. We generated a ubiquitous Pomc knockout zebrafish that mimicked the mammalian mutant phenotype of adrenal insufficiency and enhanced adiposity. The loss of Pomc inhibited stress‐induced cortisol production and reprogrammed GC signaling by reducing glucocorticoid receptor responsiveness, whereas the mineralocorticoid receptor (Mr) signaling was enhanced. Larval feeding led to enhanced growth and adipogenesis in the Pomc mutants, and this was inhibited by eplerenone, an Mr antagonist. Altogether, our results underscore a key role for Mr signaling in early developmental adipogenesis and a possible target for therapeutic intervention for early‐onset childhood obesity due to Pomc dysfunction.

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Characterization of the zebrafish (Danio rerio) mineralocorticoid receptor

Cited by 84 publications

References 38 publications

Angiotensin-II promotes Na+ uptake in larval zebrafish, Danio rerio, in acidic and ion-poor water

Angiotensin-II promotes Na+ uptake in larval zebrafish, Danio rerio, in acidic and ion-poor water

30 YEARS OF THE MINERALOCORTICOID RECEPTOR: Evolution of the mineralocorticoid receptor: sequence, structure and function

Mineralocorticoid receptor activates postnatal adiposity in zebrafish lacking proopiomelanocortin

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