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Article: Role of SCTR/AT1aR heteromer in mediating ANGII-induced aldosterone secretion

TitleRole of SCTR/AT1aR heteromer in mediating ANGII-induced aldosterone secretion
Authors
Issue Date2019
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
PLoS One, 2019, v. 14 n. 9, p. article no. e0222005 How to Cite?
AbstractThe involvement of secretin (SCT) and its receptor (SCTR) in angiotensin II (ANGII)-mediated osmoregulation by forming SCTR/ angiotensin II type 1 receptor (AT1R) heteromer is well established. In this study, we demonstrated that SCTR/AT1R complex can mediate ANGII-induced aldosterone secretion/release through potentiating calcium mobilization. Through IHC and cAMP studies, we showed the presence of functional SCTR and AT1R in the primary zona glomerulosa (ZG) cells of C57BL/6N (C57), and functional AT1R and non-functional SCTR in SCTR knockout (SCTR-/-) mice. Calcium mobilization studies revealed the important role of SCTR on ANGII-mediated calcium mobilization in adrenal gland. The fluo4-AM loaded primary adrenal ZG cells from the C57 mice displayed a dose-dependent increase in intracellular calcium influx ([Ca2+]i) when exposed to ANGII but not from the SCTR-/- ZG cells. Synthetic SCTR transmembrane (TM) peptides STM-II/-IV were able to alter [Ca2+]i in C57 mice, but not the mice with mutated STM-II/-IV (STM-IIm/IVm) peptides. Through enzyme immunoassay (EIA), we measured the aldosterone release from primary ZG cells of both C57 and SCTR-/- mice by exposing them to ANGII (10nM). SCTR-/- ZG cells showed impaired ANGII-induced aldosterone secretion compared to the C57 mice. TM peptide, STM-II hindered the aldosterone secretion in ZG cells of C57 mice. These findings support the involvement of SCTR/AT1R heterodimer complex in aldosterone secretion/release through [Ca2+]i.
Persistent Identifierhttp://hdl.handle.net/10722/276366
ISSN
2023 Impact Factor: 2.9
2023 SCImago Journal Rankings: 0.839
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorBai, J-
dc.contributor.authorDuraisamy, K-
dc.contributor.authorMak, OK-
dc.contributor.authorAllam, A-
dc.contributor.authorAjarem, J-
dc.contributor.authorZhang, L-
dc.contributor.authorChow, BKC-
dc.date.accessioned2019-09-10T03:01:43Z-
dc.date.available2019-09-10T03:01:43Z-
dc.date.issued2019-
dc.identifier.citationPLoS One, 2019, v. 14 n. 9, p. article no. e0222005-
dc.identifier.issn1932-6203-
dc.identifier.urihttp://hdl.handle.net/10722/276366-
dc.description.abstractThe involvement of secretin (SCT) and its receptor (SCTR) in angiotensin II (ANGII)-mediated osmoregulation by forming SCTR/ angiotensin II type 1 receptor (AT1R) heteromer is well established. In this study, we demonstrated that SCTR/AT1R complex can mediate ANGII-induced aldosterone secretion/release through potentiating calcium mobilization. Through IHC and cAMP studies, we showed the presence of functional SCTR and AT1R in the primary zona glomerulosa (ZG) cells of C57BL/6N (C57), and functional AT1R and non-functional SCTR in SCTR knockout (SCTR-/-) mice. Calcium mobilization studies revealed the important role of SCTR on ANGII-mediated calcium mobilization in adrenal gland. The fluo4-AM loaded primary adrenal ZG cells from the C57 mice displayed a dose-dependent increase in intracellular calcium influx ([Ca2+]i) when exposed to ANGII but not from the SCTR-/- ZG cells. Synthetic SCTR transmembrane (TM) peptides STM-II/-IV were able to alter [Ca2+]i in C57 mice, but not the mice with mutated STM-II/-IV (STM-IIm/IVm) peptides. Through enzyme immunoassay (EIA), we measured the aldosterone release from primary ZG cells of both C57 and SCTR-/- mice by exposing them to ANGII (10nM). SCTR-/- ZG cells showed impaired ANGII-induced aldosterone secretion compared to the C57 mice. TM peptide, STM-II hindered the aldosterone secretion in ZG cells of C57 mice. These findings support the involvement of SCTR/AT1R heterodimer complex in aldosterone secretion/release through [Ca2+]i.-
dc.languageeng-
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action-
dc.relation.ispartofPLoS ONE-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleRole of SCTR/AT1aR heteromer in mediating ANGII-induced aldosterone secretion-
dc.typeArticle-
dc.identifier.emailChow, BKC: bkcc@hku.hk-
dc.identifier.authorityChow, BKC=rp00681-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0222005-
dc.identifier.pmid31479491-
dc.identifier.scopuseid_2-s2.0-85071752346-
dc.identifier.hkuros305030-
dc.identifier.volume14-
dc.identifier.issue9-
dc.identifier.spagearticle no. e0222005-
dc.identifier.epagearticle no. e0222005-
dc.identifier.isiWOS:000486302400038-
dc.publisher.placeUnited States-
dc.identifier.issnl1932-6203-

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