Performing a hepatic timing signal: glucocorticoids induce gper1a and gper1b expression and repress gclock1a and gbmal1a in the liver of goldfish

Simple item page
dc.contributor.authorSánchez Bretaño, Aída
dc.contributor.authorCallejo, María
dc.contributor.authorMontero, Marta
dc.contributor.authorAlonso Gómez, Ángel L.
dc.contributor.authorDelgado Saavedra, María Jesús
dc.contributor.authorIsorna Alonso, Esther
dc.date.accessioned2023-06-18T05:47:40Z
dc.date.available2023-06-18T05:47:40Z
dc.date.issued2016
dc.description.abstractGlucocorticoids have been recently proposed as input signals of circadian system, although the underlying molecular mechanism remains unclear. This work investigates the role of glucocorticoids as modulators of clock genes expression in the liver of goldfish. In fish maintained under a 12L:12D photoperiod, an intraperitoneal injection at Zeitgeber Time 2 of a glucocorticoid analog, dexamethasone (1 μg/g body weight) induced per1 genes while decreased gbmal1a and gclock1a expression in the liver at 8 h post-injection. A 4-h in vitro exposure of goldfish liver to cortisol (0.1–10 μM) also induced gper1 genes in a concentration-dependent manner. Similarly, the exposure of the goldfish cultured liver to dexamethasone produced a concentration-dependent induction of gper1 genes. Moreover, this glucocorticoid analog led to a decrease in gbmal1a and gclock1a transcripts, while the other clock genes analyzed were unaffected. The induction of gper1a and gper1b by dexamethasone in vitro was observed at short times (2 h), whereas the reductions of gbmal1a and gclock1a transcripts needed longer exposure times (8 h) to the glucocorticoid to be significant. Additionally, a 2-h exposure to dexamethasone in the liver culture was enough to extend the induction of per genes for more than 12 h. Present results indicate that gper1 genes are targets for glucocorticoids in the regulation of goldfish hepatic oscillator, as previously reported in mammals, suggesting a conserved role of glucocorticoids in the functional organization of the peripheral circadian system in vertebrates. The repression of clock1a and bmal1a is not so well established, and suggests that other clock genes could be glucocorticoid targets in the goldfish liver.
dc.description.departmentDepto. de Genética, Fisiología y Microbiología
dc.description.facultyFac. de Ciencias Biológicas
dc.description.refereedTRUE
dc.description.sponsorshipMinisterio de Economía y Competitividad (MINECO)
dc.description.statuspub
dc.eprint.idhttps://eprints.ucm.es/id/eprint/42706
dc.identifier.doi10.1007/s00360-015-0936-2
dc.identifier.issn0174-1578
dc.identifier.officialurlhttps://link.springer.com/journal/360
dc.identifier.urihttps://hdl.handle.net/20.500.14352/23351
dc.issue.number1
dc.journal.titleJournal of Comparative Physiology B
dc.language.isoeng
dc.page.final82
dc.page.initial73
dc.publisherSpringer Link
dc.relation.projectIDAGL2013-46448-C3-2-R
dc.relation.projectIDFPI Grant BES-2011-047620
dc.rights.accessRightsrestricted access
dc.subject.cdu591.1
dc.subject.cdu597.2/.5
dc.subject.keywordCortisol
dc.subject.keywordDexamethasone
dc.subject.keywordLiver
dc.subject.keywordCircadian system
dc.subject.keywordClock genes
dc.subject.keywordper1
dc.subject.keywordTeleosts
dc.subject.ucmBiología
dc.subject.ucmFisiología animal (Biología)
dc.subject.ucmPeces
dc.subject.unesco24 Ciencias de la Vida
dc.subject.unesco2401.13 Fisiología Animal
dc.titlePerforming a hepatic timing signal: glucocorticoids induce gper1a and gper1b expression and repress gclock1a and gbmal1a in the liver of goldfish
dc.typejournal article
dc.volume.number186
dspace.entity.typePublication
relation.isAuthorOfPublication48071251-a236-4607-ab33-5332c1472628
relation.isAuthorOfPublication882d1fb3-a920-418a-9f3f-1b8f6b967032
relation.isAuthorOfPublication.latestForDiscovery48071251-a236-4607-ab33-5332c1472628
Download
Original bundle
Now showing 1 - 1 of 1
No Thumbnail Available
Name:
callejo.2016.Performing a hepatic timing signal.pdf
Size:
1.03 MB
Format:
Adobe Portable Document Format
Download
Collections
Artículos