Identification of glucocorticoid receptors as potential modulators of parasympathetic and sympathetic neurons within rat intracardiac ganglia.
corticosteroid receptors
intracardiac ganglia
parasympathetic
sensory nerves
sympathetic
Journal
Frontiers in neuroanatomy
ISSN: 1662-5129
Titre abrégé: Front Neuroanat
Pays: Switzerland
ID NLM: 101477943
Informations de publication
Date de publication:
2022
2022
Historique:
received:
23
03
2022
accepted:
07
09
2022
entrez:
10
10
2022
pubmed:
11
10
2022
medline:
11
10
2022
Statut:
epublish
Résumé
Emerging evidences indicate that glucocorticoid receptors (GR) play a regulatory role in cardiac function, particularly with regard to the autonomic nervous system. Therefore, this study aimed to demonstrate the expression and the precise anatomical location of GR in relation to the parasympathetic and sympathetic innervations of the heart. The present study used tissue samples from rat heart atria to perform conventional reverse-transcriptase polymerase chain reaction (RT-PCR), Western blot, and double immunofluorescence confocal analysis of GR with the neuronal markers vesicular acetylcholine transporter (VAChT), tyrosine hydroxylase (TH), calcitonin gene-related peptide (CGRP) as well as the mineralocorticoid receptor (MR). Double immunofluorescence labeling revealed that GRs were co-expressed with VAChT in parasympathetic principal neuronal somata and nerve terminals innervating atrium. Also, GR colocalized with the sympathetic neuronal marker TH in a cluster of small intensely fluorescent (SIF) cells, on intracardiac nerve terminals and in the atrial myocardium. GR immunoreactivity was scarcely identified on CGRP-immunoreactive sensory nerve terminals. Approximately 20% of GR immunoreactive neuronal somata co-localized with MR. Finally, conventional RT-PCR and Western blot confirmed the presence of GR and MR in rat heart atria. This study provides evidence for the existence of GR predominantly on cardiac parasympathetic neurons and TH-immunoreactive SIF cells suggesting a functional role of cardiac GR on cardiovascular function by modulation of the cardiac autonomic nervous system.
Sections du résumé
Background
UNASSIGNED
Emerging evidences indicate that glucocorticoid receptors (GR) play a regulatory role in cardiac function, particularly with regard to the autonomic nervous system. Therefore, this study aimed to demonstrate the expression and the precise anatomical location of GR in relation to the parasympathetic and sympathetic innervations of the heart.
Methods
UNASSIGNED
The present study used tissue samples from rat heart atria to perform conventional reverse-transcriptase polymerase chain reaction (RT-PCR), Western blot, and double immunofluorescence confocal analysis of GR with the neuronal markers vesicular acetylcholine transporter (VAChT), tyrosine hydroxylase (TH), calcitonin gene-related peptide (CGRP) as well as the mineralocorticoid receptor (MR).
Results
UNASSIGNED
Double immunofluorescence labeling revealed that GRs were co-expressed with VAChT in parasympathetic principal neuronal somata and nerve terminals innervating atrium. Also, GR colocalized with the sympathetic neuronal marker TH in a cluster of small intensely fluorescent (SIF) cells, on intracardiac nerve terminals and in the atrial myocardium. GR immunoreactivity was scarcely identified on CGRP-immunoreactive sensory nerve terminals. Approximately 20% of GR immunoreactive neuronal somata co-localized with MR. Finally, conventional RT-PCR and Western blot confirmed the presence of GR and MR in rat heart atria.
Conclusion
UNASSIGNED
This study provides evidence for the existence of GR predominantly on cardiac parasympathetic neurons and TH-immunoreactive SIF cells suggesting a functional role of cardiac GR on cardiovascular function by modulation of the cardiac autonomic nervous system.
Identifiants
pubmed: 36213610
doi: 10.3389/fnana.2022.902738
pmc: PMC9539283
doi:
Types de publication
Journal Article
Langues
eng
Pagination
902738Informations de copyright
Copyright © 2022 Mousa, Dehe, Aboryag, Shaqura, Beyer, Schäfer and Treskatsch.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Références
Early Hum Dev. 2004 Jan;76(1):65-77
pubmed: 14729164
Mol Endocrinol. 1989 Oct;3(10):1674-80
pubmed: 2608053
Science. 1987 Jul 17;237(4812):268-75
pubmed: 3037703
Microsc Res Tech. 1994 Oct 1;29(2):143-50
pubmed: 7812035
J Endocrinol. 2019 Jun 1;241(3):279-292
pubmed: 31013474
Neurosci Res. 2005 Apr;51(4):371-81
pubmed: 15740800
J Steroid Biochem Mol Biol. 2015 Sep;153:27-34
pubmed: 25804222
Diabetes Res Clin Pract. 2010 Feb;87(2):184-91
pubmed: 19962776
Endocrinology. 1997 Mar;138(3):1305-11
pubmed: 9048640
Brain. 2007 Feb;130(Pt 2):502-13
pubmed: 17142830
J Comp Neurol. 2010 Sep 15;518(18):3836-47
pubmed: 20653037
Obstet Gynecol. 2009 May;113(5):1082-1088
pubmed: 19384124
Steroids. 2011 Dec 20;76(14):1541-5
pubmed: 21945398
Front Endocrinol (Lausanne). 2020 May 27;11:347
pubmed: 32528419
Endocrinology. 2006 Mar;147(3):1343-8
pubmed: 16293659
Mediators Inflamm. 2017;2017:9243736
pubmed: 28316377
Am J Physiol. 1991 Feb;260(2 Pt 1):C226-33
pubmed: 1847584
J Mol Cell Cardiol. 2018 Jun;119:1-9
pubmed: 29653111
Neuropharmacology. 2016 Aug;107:251-261
pubmed: 27016023
Postgrad Med J. 1985 Jun;61(716):501-3
pubmed: 4011533
Am J Physiol Regul Integr Comp Physiol. 2006 Apr;290(4):R1003-11
pubmed: 16269575
J Virol. 2017 Jun 9;91(13):
pubmed: 28404850
J Am Soc Hypertens. 2018 Aug;12(8):605-613
pubmed: 29945776
Brain Res. 2019 Jun 1;1712:180-187
pubmed: 30771315
J Lab Clin Med. 1992 Dec;120(6):893-901
pubmed: 1453111
Am J Physiol Regul Integr Comp Physiol. 2001 May;280(5):R1440-9
pubmed: 11294766
J Physiol. 1976 Jan;254(2):405-25
pubmed: 1249783
Am J Physiol Regul Integr Comp Physiol. 2001 Mar;280(3):R646-54
pubmed: 11171641
J Allergy Clin Immunol. 2013 Nov;132(5):1033-44
pubmed: 24084075
Anesthesiology. 2018 Apr;128(4):796-809
pubmed: 29356757
Am J Physiol Renal Physiol. 2001 Feb;280(2):F181-92
pubmed: 11208593
J Mol Endocrinol. 2017 Jan;58(1):R1-R13
pubmed: 27553202
J Clin Endocrinol Metab. 1995 Jun;80(6):1804-8
pubmed: 7775627
Nat Rev Cardiol. 2022 Sep;19(9):574
pubmed: 35831539
Front Neuroanat. 2022 Jan 11;15:802359
pubmed: 35087382
Neuropharmacology. 2016 Dec;111:1-13
pubmed: 27558347
Anesthesiology. 2020 Apr;132(4):867-880
pubmed: 32011337
Trends Endocrinol Metab. 2016 Jan;27(1):35-43
pubmed: 26586027
Br J Obstet Gynaecol. 1994 Aug;101(8):675-9
pubmed: 7947501
J Neurosci. 1985 Aug;5(8):2143-60
pubmed: 4020433
N Engl J Med. 2001 Dec 6;345(23):1689-97
pubmed: 11759649
Am J Physiol Regul Integr Comp Physiol. 2002 Feb;282(2):R475-83
pubmed: 11792657
Pediatr Res. 1995 Oct;38(4):479-84
pubmed: 8559597
Hum Mol Genet. 2013 Aug 15;22(16):3269-82
pubmed: 23595884
Basic Res Cardiol. 2019 Oct 31;114(6):47
pubmed: 31673803
Sci Signal. 2019 Apr 16;12(577):
pubmed: 30992401
Nat Methods. 2012 Jul;9(7):671-5
pubmed: 22930834
Endocrinology. 1992 Sep;131(3):1369-76
pubmed: 1505468
J Comp Neurol. 2011 Apr 1;519(5):957-71
pubmed: 21280046
J Am Heart Assoc. 2019 Aug 6;8(15):e011012
pubmed: 31311395