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. 2019 Jan;112(1):67-75.
doi: 10.5935/abc.20190001. Epub 2018 Dec 13.

Sex-Related Effects of Prenatal Stress on Region-Specific Expression of Monoamine Oxidase A and β Adrenergic Receptors in Rat Hearts

[Article in English, Portuguese]
Tanja Jevjdovic  1 , Tamara Dakic  1 , Sonja Kopanja  2 , Iva Lakic  1 , Predrag Vujovic  1 , Nebojsa Jasnic  1 , Jelena Djordjevic  1
Affiliations

Sex-Related Effects of Prenatal Stress on Region-Specific Expression of Monoamine Oxidase A and β Adrenergic Receptors in Rat Hearts

[Article in English, Portuguese]
Tanja Jevjdovic et al. Arq Bras Cardiol. 2019 Jan.

Erratum in

  • Erratum.
    [No authors listed] [No authors listed] Arq Bras Cardiol. 2019 Feb;112(2):214. doi: 10.5935/abc.20190019. Arq Bras Cardiol. 2019. PMID: 30785589 Free PMC article.

Abstract

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.

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Conflict of interest statement

Potential Conflict of Interest

No potential conflict of interest relevant to this article was reported.

Figures

Figure 1
Figure 1
Maternal plasma ACTH concentrations before (GD13) and following (GD21) exposure to CUMS during pregnancy. Data are expressed as mean ± SD, control group (open bars, n =5), stressed group (black bars, n = 6). In the stressed group on GD21 two samples were excluded due to hemolysis. ***p < 0.001, 2-way ANOVA and Bonferroni's multiple comparison test
Figure 2
Figure 2
Effects of prenatal stress on expression of beta 1 (ADRB1) and beta 2 (ADRB2) adrenergic receptors mRNA at the apex and base of the left ventricle in the offspring (LV). Results are presented for female (A and C) and male (B and D) offspring from unstressed (control-C) and stressed mothers (prenatal stress-PS). Data are expressed as median with interquartile range (number of animals per group, n = 5-8 per group). *p < 0.05; **p < 0.01, Mann-Whitney U-test
Figure 3
Figure 3
Effects of prenatal stress on monoamine oxidase A (MAO-A) mRNA at the apex and base of the left ventricle (LV) in the offspring. Results are presented for female (A and C) and male (B and D) offspring from unstressed (control-C) and stressed mothers (prenatal stress-PS). Data are expressed as median with interquartile range (number of animals per group, n = 5-8).
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Comment in

References

    1. Dong M, Zheng Q, Ford SP, Nathanielsz PW, Ren J. Maternal obesity, lipotoxicity and cardiovascular diseases in offspring. J Mol Cell Cardiol. 2013 Feb;55:111–116. - PubMed
    1. Roseboom TJ, van der Meulen JH, Osmond C, Barker DJ, Ravelli AC, Schroeder-Tanka JM, et al. Coronary heart disease after prenatal exposure to the Dutch famine, 1944-45. Heart. 2000;84(6):595–598. - PMC - PubMed
    1. Hoet JJ, Hanson MA. Intrauterine nutrition: its importance during critical periods for cardiovascular and endocrine development. J Physiol. 1999;514(3):617–627. - PMC - PubMed
    1. Bertram CE, Hanson MA. Prenatal programming of postnatal endocrine responses by glucocorticoids. Reproduction. 2002;124(4):459–467. - PubMed
    1. Igosheva N, Klimova O, Anishchenko T, Glover V. Prenatal stress alters cardiovascular responses in adult rats. J Physiol. 2004;557(1):273–285. - PMC - PubMed

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