دورية أكاديمية
أعرض في EDS

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

التفاصيل البيبلوغرافية
العنوان: Role of SCTR/AT1aR heteromer in mediating ANGII-induced aldosterone secretion.
المؤلفون: Bai J; School of Biological Sciences, University of Hong Kong, Hong Kong, China., Duraisamy K; School of Biological Sciences, University of Hong Kong, Hong Kong, China., Mak SOK; School of Biological Sciences, University of Hong Kong, Hong Kong, China., Allam A; Department of Zoology, College of Science, King Saud University, Riyadh, KSA.; Department of Zoology, Faculty of Science, Beni-Suef University, Beni-Suef, Egypt., Ajarem J; Department of Zoology, College of Science, King Saud University, Riyadh, KSA., Li Z; GHM Institute of CNS Regeneration, Jinan University, Guangzhou, China., Chow BKC; School of Biological Sciences, University of Hong Kong, Hong Kong, China.
المصدر: PloS one [PLoS One] 2019 Sep 03; Vol. 14 (9), pp. e0222005. Date of Electronic Publication: 2019 Sep 03 (Print Publication: 2019).
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
أسماء مطبوعة: Original Publication: San Francisco, CA : Public Library of Science
مواضيع طبية MeSH: Aldosterone/*metabolism , Angiotensin II/*metabolism , Receptor, Angiotensin, Type 1/*metabolism , Receptors, G-Protein-Coupled/*metabolism , Receptors, Gastrointestinal Hormone/*metabolism, Animals ; Calcium Signaling ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mutation ; Osmoregulation/genetics ; Osmoregulation/physiology ; Peptide Fragments/chemistry ; Peptide Fragments/genetics ; Peptide Fragments/metabolism ; Protein Structure, Quaternary ; Receptor, Angiotensin, Type 1/chemistry ; Receptors, G-Protein-Coupled/chemistry ; Receptors, G-Protein-Coupled/deficiency ; Receptors, Gastrointestinal Hormone/chemistry ; Receptors, Gastrointestinal Hormone/deficiency ; Zona Glomerulosa/cytology ; Zona Glomerulosa/metabolism
مستخلص: The 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.
Competing Interests: The authors have declared that no competing interests exist.
References: Regul Pept. 1999 Apr 30;80(3):91-100. (PMID: 10425651)
Pharmacol Rev. 2000 Sep;52(3):415-72. (PMID: 10977869)
Toxicol Pathol. 2001 Jan-Feb;29(1):41-8. (PMID: 11215683)
Sci STKE. 2003 May 06;2003(181):PE16. (PMID: 12734384)
Mol Endocrinol. 2004 Feb;18(2):279-90. (PMID: 14645496)
Mol Cell Endocrinol. 2004 Mar 31;217(1-2):67-74. (PMID: 15134803)
Physiol Genomics. 2004 Sep 16;19(1):106-16. (PMID: 15375197)
Endocr Rev. 2004 Dec;25(6):947-70. (PMID: 15583024)
J Endocrinol. 2005 Jul;186(1):1-20. (PMID: 16002531)
J Pediatr Surg. 2006 Dec;41(12):2008-12. (PMID: 17161193)
Mol Cell Biol. 2007 Apr;27(7):2499-511. (PMID: 17283064)
Physiol Genomics. 2007 Jun 19;30(1):26-34. (PMID: 17327493)
Nat Protoc. 2008;3(6):1101-8. (PMID: 18546601)
J Mol Endocrinol. 2009 Apr;42(4):319-30. (PMID: 19158234)
FASEB J. 2010 Dec;24(12):5024-32. (PMID: 20739612)
Annu Rev Physiol. 2011;73:335-57. (PMID: 20809792)
Hypertension. 2010 Nov;56(5):885-92. (PMID: 20937967)
Mol Cell Endocrinol. 2012 Mar 24;350(2):151-62. (PMID: 21839803)
Biochim Biophys Acta. 2013 Jul;1828(7):1550-9. (PMID: 22975282)
Pharmacol Rev. 2013 Mar 13;65(2):809-48. (PMID: 23487168)
Int J Hypertens. 2013;2013:175428. (PMID: 23573410)
FASEB J. 2014 Jun;28(6):2632-44. (PMID: 24599969)
Mol Cell Biol. 2014 Oct;34(20):3880-94. (PMID: 25092869)
J Hum Hypertens. 2015 Sep;29(9):515-21. (PMID: 25631218)
FASEB J. 2017 Apr;31(4):1689-1697. (PMID: 28082350)
FASEB J. 2019 Apr;33(4):5389-5398. (PMID: 30702925)
Blood Press Suppl. 1994;5:109-12. (PMID: 7889191)
Hypertension. 1994 Nov;24(5):531-7. (PMID: 7960011)
Endocrinology. 1994 Aug;135(2):751-8. (PMID: 8033823)
Am J Physiol. 1994 Aug;267(2 Pt 1):E260-7. (PMID: 8074205)
J Biol Chem. 1996 Sep 6;271(36):22063-9. (PMID: 8703014)
Regul Pept. 1995 Dec 14;60(2-3):135-47. (PMID: 8746540)
المشرفين على المادة: 0 (Peptide Fragments)
0 (Receptor, Angiotensin, Type 1)
0 (Receptors, G-Protein-Coupled)
0 (Receptors, Gastrointestinal Hormone)
0 (secretin receptor)
11128-99-7 (Angiotensin II)
4964P6T9RB (Aldosterone)
تواريخ الأحداث: Date Created: 20190904 Date Completed: 20200316 Latest Revision: 20200316
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC6719825
DOI: 10.1371/journal.pone.0222005
PMID: 31479491
قاعدة البيانات: MEDLINE
الوصف
تدمد:1932-6203
DOI:10.1371/journal.pone.0222005