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Article: IGFs potentiate TAC3-induced SLα expression via upregulation of TACR3 expression in grass carp pituitary cells

TitleIGFs potentiate TAC3-induced SLα expression via upregulation of TACR3 expression in grass carp pituitary cells
Authors
Keywordssignal transduction
tachykinin receptor
pharmacological test
neurokinin B
grass carp
Issue Date2019
PublisherMDPI AG. The Journal's web site is located at http://www.mdpi.com/journal/cells
Citation
Cells, 2019, v. 8 n. 8, p. article no. 887 How to Cite?
AbstractIn mammals, the tachykinin 3 (TAC3)/tachykinin receptor 3 (TACR3) systems have been confirmed to play an important role in the regulation of puberty onset. Using grass carp pituitary cells as the model, our recent study found that the TAC3 gene products could significantly induce somatolactin α (SLα) synthesis and secretion via TACR3 activation. In the present study, we seek to examine if pituitary TACR3 can serve as a regulatory target and contribute to TAC3 interactions with other SLα regulators. Firstly, grass carp TACR3 was cloned and tissue distribution showed that it could be highly detected in grass carp pituitary. Using HEK293 cells as the model, functional expression also revealed that grass carp TACR3 exhibited ligand binding selectivity and post-receptor signaling highly comparable to its mammalian counterpart. Using grass carp pituitary cells as the model, TACR3 mRNA expression could be stimulated by insulin-like growth factor (IGF)-I and -II via the IGF-I receptor coupled to phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) and mitogen-activated protein kinase (MAPK) pathways. Interestingly, IGF-I/-II cotreatment could also significantly enhance TAC3-induced SLα mRNA expression and the potentiating effect was dependent on TACR3 expression and activation of adenylate cyclase (AC)/cAMP/protein kinase A (PKA), phospholipase C (PLC)/inositol 1,4,5-triphosphate (IP3)/protein kinase C (PKC), and Ca2+/calmodulin (CaM)/calmodulin-dependent protein kinase II (CaMK-II) cascades. Besides, IGF-I-induced Akt phosphorylation but not MEK, extracellular signal-regulated kinase (ERK1/2), and P38MAPK phosphorylation was notably enhanced by TACR3 activation. These results, as a whole, suggest that the potentiating effect of IGFs on TAC3 gene products-induced SLα mRNA expression was mediated by TACR3 upregulation and functional crosstalk of post-receptor signaling in the pituitary.
Persistent Identifierhttp://hdl.handle.net/10722/277894
ISSN
2017 Impact Factor: 4.829
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHu, G-
dc.contributor.authorHe, M-
dc.contributor.authorKo, KW-
dc.contributor.authorYe, C-
dc.contributor.authorHu, Q-
dc.contributor.authorWong, AOL-
dc.date.accessioned2019-10-04T08:03:27Z-
dc.date.available2019-10-04T08:03:27Z-
dc.date.issued2019-
dc.identifier.citationCells, 2019, v. 8 n. 8, p. article no. 887-
dc.identifier.issn2073-4409-
dc.identifier.urihttp://hdl.handle.net/10722/277894-
dc.description.abstractIn mammals, the tachykinin 3 (TAC3)/tachykinin receptor 3 (TACR3) systems have been confirmed to play an important role in the regulation of puberty onset. Using grass carp pituitary cells as the model, our recent study found that the TAC3 gene products could significantly induce somatolactin α (SLα) synthesis and secretion via TACR3 activation. In the present study, we seek to examine if pituitary TACR3 can serve as a regulatory target and contribute to TAC3 interactions with other SLα regulators. Firstly, grass carp TACR3 was cloned and tissue distribution showed that it could be highly detected in grass carp pituitary. Using HEK293 cells as the model, functional expression also revealed that grass carp TACR3 exhibited ligand binding selectivity and post-receptor signaling highly comparable to its mammalian counterpart. Using grass carp pituitary cells as the model, TACR3 mRNA expression could be stimulated by insulin-like growth factor (IGF)-I and -II via the IGF-I receptor coupled to phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) and mitogen-activated protein kinase (MAPK) pathways. Interestingly, IGF-I/-II cotreatment could also significantly enhance TAC3-induced SLα mRNA expression and the potentiating effect was dependent on TACR3 expression and activation of adenylate cyclase (AC)/cAMP/protein kinase A (PKA), phospholipase C (PLC)/inositol 1,4,5-triphosphate (IP3)/protein kinase C (PKC), and Ca2+/calmodulin (CaM)/calmodulin-dependent protein kinase II (CaMK-II) cascades. Besides, IGF-I-induced Akt phosphorylation but not MEK, extracellular signal-regulated kinase (ERK1/2), and P38MAPK phosphorylation was notably enhanced by TACR3 activation. These results, as a whole, suggest that the potentiating effect of IGFs on TAC3 gene products-induced SLα mRNA expression was mediated by TACR3 upregulation and functional crosstalk of post-receptor signaling in the pituitary.-
dc.languageeng-
dc.publisherMDPI AG. The Journal's web site is located at http://www.mdpi.com/journal/cells-
dc.relation.ispartofCells-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectsignal transduction-
dc.subjecttachykinin receptor-
dc.subjectpharmacological test-
dc.subjectneurokinin B-
dc.subjectgrass carp-
dc.titleIGFs potentiate TAC3-induced SLα expression via upregulation of TACR3 expression in grass carp pituitary cells-
dc.typeArticle-
dc.identifier.emailHe, M: hemu@hkucc.hku.hk-
dc.identifier.emailKo, KW: wendyko@hku.hk-
dc.identifier.emailWong, AOL: olwong@hku.hk-
dc.identifier.authorityWong, AOL=rp00806-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3390/cells8080887-
dc.identifier.pmid31412674-
dc.identifier.pmcidPMC6721824-
dc.identifier.hkuros306497-
dc.identifier.volume8-
dc.identifier.issue8-
dc.identifier.spagearticle no. 887-
dc.identifier.epagearticle no. 887-
dc.identifier.isiWOS:000484537500120-
dc.publisher.placeSwitzerland-

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