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Article: Medaka osmotic stress transcription factor 1b (Ostf1b/TSC22D3-2) triggers hyperosmotic responses of different ion transporters in medaka gill and human embryonic kidney cells via the JNK signalling pathway

TitleMedaka osmotic stress transcription factor 1b (Ostf1b/TSC22D3-2) triggers hyperosmotic responses of different ion transporters in medaka gill and human embryonic kidney cells via the JNK signalling pathway
Authors
Issue Date2011
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/biocel
Citation
International Journal Of Biochemistry And Cell Biology, 2011, v. 43 n. 12, p. 1764-1775 How to Cite?
AbstractEukaryotic cells undergo rapid regulatory processes to maintain cellular homeostasis upon osmotic stress. In fishes, gill epithelial cells play main roles in these processes. Although osmoregulatory functions of fish gills have been well studied, little is known about the underlying mechanisms, particularly the hypertonic-induced signalling pathways during osmotic stress. This study reports for the first time on the osmo-sensing signal cascade that related to the medaka osmotic stress transcription factor 1 (Ostf1), a hypertonic induced immediate early gene, under hypertonic stress. Quantitative real-time PCR showed the rapid increase of Ostf1 in gill after transfer of medaka from fresh water to 50% seawater; particularly Ostf1b whose mRNA expression increased to 4 folds at 0.5 h and reached to 10 folds at 6 h after the transfer. The in vivo knockdown of Ostf1b profoundly inhibited SEK and JNK phosphorylation, but not p38 and ERK phosphorylation in the medaka gill tissue. To further investigate the possible role of Ostf1b in the JNK pathway, Ostf1b was ectopically expressed in HEK293 cells. Results indicated that Ostf1b is a downstream target of SEK and JNK and exerts a positive feedback loop on the JNK signalling pathway via activation of GCK and/or MLK3 proteins. Additionally, MAPK inhibitors experiments suggested that activation of the JNK pathway by hypertonicity is involved in the maintenance of Ostf1b stability, which in turn provides continuous stimulation of GCK for JNK phosphorylation. Lastly, changes in transcription levels of different water/ion transporters were found in knockdown or ecoptic over-expression of Ostf1b in medaka gills and human embryonic kidney cells, suggesting the role of Ostf1b in modulation of critical water channel/ion transporters during osmotic stress. © 2011 Elsevier Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/183402
ISSN
2015 Impact Factor: 3.905
2015 SCImago Journal Rankings: 2.003
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTse, WKFen_US
dc.contributor.authorLai, KPen_US
dc.contributor.authorTakei, Yen_US
dc.date.accessioned2013-05-27T07:12:37Z-
dc.date.available2013-05-27T07:12:37Z-
dc.date.issued2011en_US
dc.identifier.citationInternational Journal Of Biochemistry And Cell Biology, 2011, v. 43 n. 12, p. 1764-1775en_US
dc.identifier.issn1357-2725en_US
dc.identifier.urihttp://hdl.handle.net/10722/183402-
dc.description.abstractEukaryotic cells undergo rapid regulatory processes to maintain cellular homeostasis upon osmotic stress. In fishes, gill epithelial cells play main roles in these processes. Although osmoregulatory functions of fish gills have been well studied, little is known about the underlying mechanisms, particularly the hypertonic-induced signalling pathways during osmotic stress. This study reports for the first time on the osmo-sensing signal cascade that related to the medaka osmotic stress transcription factor 1 (Ostf1), a hypertonic induced immediate early gene, under hypertonic stress. Quantitative real-time PCR showed the rapid increase of Ostf1 in gill after transfer of medaka from fresh water to 50% seawater; particularly Ostf1b whose mRNA expression increased to 4 folds at 0.5 h and reached to 10 folds at 6 h after the transfer. The in vivo knockdown of Ostf1b profoundly inhibited SEK and JNK phosphorylation, but not p38 and ERK phosphorylation in the medaka gill tissue. To further investigate the possible role of Ostf1b in the JNK pathway, Ostf1b was ectopically expressed in HEK293 cells. Results indicated that Ostf1b is a downstream target of SEK and JNK and exerts a positive feedback loop on the JNK signalling pathway via activation of GCK and/or MLK3 proteins. Additionally, MAPK inhibitors experiments suggested that activation of the JNK pathway by hypertonicity is involved in the maintenance of Ostf1b stability, which in turn provides continuous stimulation of GCK for JNK phosphorylation. Lastly, changes in transcription levels of different water/ion transporters were found in knockdown or ecoptic over-expression of Ostf1b in medaka gills and human embryonic kidney cells, suggesting the role of Ostf1b in modulation of critical water channel/ion transporters during osmotic stress. © 2011 Elsevier Ltd.en_US
dc.languageengen_US
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/biocelen_US
dc.relation.ispartofInternational Journal of Biochemistry and Cell Biologyen_US
dc.subject.meshAmino Acid Sequenceen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshFish Proteins - Genetics - Metabolismen_US
dc.subject.meshGene Expression Regulationen_US
dc.subject.meshGills - Metabolismen_US
dc.subject.meshHek293 Cellsen_US
dc.subject.meshHumansen_US
dc.subject.meshIon Transporten_US
dc.subject.meshMap Kinase Signaling Systemen_US
dc.subject.meshMembrane Transport Proteins - Genetics - Metabolismen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshOryzias - Genetics - Metabolismen_US
dc.subject.meshOsmosis - Physiologyen_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshReal-Time Polymerase Chain Reactionen_US
dc.subject.meshTranscription Factors - Genetics - Metabolismen_US
dc.titleMedaka osmotic stress transcription factor 1b (Ostf1b/TSC22D3-2) triggers hyperosmotic responses of different ion transporters in medaka gill and human embryonic kidney cells via the JNK signalling pathwayen_US
dc.typeArticleen_US
dc.identifier.emailLai, KP: ballllai@hotmail.comen_US
dc.identifier.authorityLai, KP=rp01753en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.biocel.2011.08.013en_US
dc.identifier.pmid21907305-
dc.identifier.scopuseid_2-s2.0-80255123841en_US
dc.identifier.hkuros223759-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80255123841&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume43en_US
dc.identifier.issue12en_US
dc.identifier.spage1764en_US
dc.identifier.epage1775en_US
dc.identifier.isiWOS:000297491700015-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridTse, WKF=11438835100en_US
dc.identifier.scopusauthoridLai, KP=7402135707en_US
dc.identifier.scopusauthoridTakei, Y=7202470685en_US

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