Sex-Related Effects of Prenatal Stress on Region-Specific Expression of Monoamine Oxidase A and β Adrenergic Receptors in Rat Hearts.
Adrenocorticotropic Hormone
/ blood
Animals
Cardiovascular Diseases
/ etiology
Female
Gene Expression
Heart Ventricles
/ metabolism
Monoamine Oxidase
/ analysis
Mothers
/ psychology
Myocardium
/ metabolism
Pregnancy
Pregnancy, Animal
/ psychology
Prenatal Exposure Delayed Effects
/ metabolism
RNA, Messenger
/ analysis
Rats, Wistar
Real-Time Polymerase Chain Reaction
Receptors, Adrenergic, beta
/ analysis
Reference Values
Sex Factors
Stress, Psychological
/ genetics
Time Factors
Journal
Arquivos brasileiros de cardiologia
ISSN: 1678-4170
Titre abrégé: Arq Bras Cardiol
Pays: Brazil
ID NLM: 0421031
Informations de publication
Date de publication:
01 2019
01 2019
Historique:
received:
01
02
2018
accepted:
23
07
2018
pubmed:
21
12
2018
medline:
18
12
2019
entrez:
21
12
2018
Statut:
ppublish
Résumé
Prenatal stress may increase risk of developing cardiovascular disorders in adulthood. The cardiotoxic effects of catecholamines are mediated via prolonged adrenergic receptor stimulation and increased oxidative stress upon their degradation by monoamine oxidase A (MAO-A). We investigated long-term effects of prenatal stress on β (1, 2, 3) adrenergic receptors and MAO-A gene expression in the hearts of adult rat offspring. Pregnant rats were exposed to unpredictable mild stress during the third week of gestation. RNA was isolated from left ventricular apex and base of adult offspring. Quantitative PCR was used to measure gene expression in collected ventricular tissue samples. The level of significance was set to p < 0.05. β3 adrenergic receptor mRNA was undetectable in rat left ventricle. β1 adrenergic receptor was the predominantly expressed subtype at the apical and basal left ventricular myocardium in the control females. Male offspring from unstressed mothers displayed higher apical cardiac β1 than β2 adrenergic receptor mRNA levels. However, β1 and β2 adrenergic receptor mRNAs were similarly expressed at the ventricular basal myocardium in males. Unlike males, prenatally stressed females exhibited decreased β1 adrenergic receptor mRNA expression at the apical myocardium. Prenatal stress did not affect cardiac MAO-A gene expression. Collectively, our results show that prenatal stress may have exerted region- and sex-specific β1 and β2 adrenergic receptor expression patterns within the left ventricle.
Sections du résumé
BACKGROUND
Prenatal stress may increase risk of developing cardiovascular disorders in adulthood. The cardiotoxic effects of catecholamines are mediated via prolonged adrenergic receptor stimulation and increased oxidative stress upon their degradation by monoamine oxidase A (MAO-A).
OBJECTIVES
We investigated long-term effects of prenatal stress on β (1, 2, 3) adrenergic receptors and MAO-A gene expression in the hearts of adult rat offspring.
METHODS
Pregnant rats were exposed to unpredictable mild stress during the third week of gestation. RNA was isolated from left ventricular apex and base of adult offspring. Quantitative PCR was used to measure gene expression in collected ventricular tissue samples. The level of significance was set to p < 0.05.
RESULTS
β3 adrenergic receptor mRNA was undetectable in rat left ventricle. β1 adrenergic receptor was the predominantly expressed subtype at the apical and basal left ventricular myocardium in the control females. Male offspring from unstressed mothers displayed higher apical cardiac β1 than β2 adrenergic receptor mRNA levels. However, β1 and β2 adrenergic receptor mRNAs were similarly expressed at the ventricular basal myocardium in males. Unlike males, prenatally stressed females exhibited decreased β1 adrenergic receptor mRNA expression at the apical myocardium. Prenatal stress did not affect cardiac MAO-A gene expression.
CONCLUSIONS
Collectively, our results show that prenatal stress may have exerted region- and sex-specific β1 and β2 adrenergic receptor expression patterns within the left ventricle.
Identifiants
pubmed: 30569948
pii: S0066-782X2018005018102
doi: 10.5935/abc.20190001
pmc: PMC6317614
pii:
doi:
Substances chimiques
RNA, Messenger
0
Receptors, Adrenergic, beta
0
Adrenocorticotropic Hormone
9002-60-2
Monoamine Oxidase
EC 1.4.3.4
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
por
Sous-ensembles de citation
IM
Pagination
67-75Commentaires et corrections
Type : CommentIn
Type : ErratumIn
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