Hostname: page-component-76fb5796d-skm99 Total loading time: 0 Render date: 2024-04-28T07:41:54.463Z Has data issue: false hasContentIssue false
  • English
  • Français

Effect of a low-protein diet during pregnancy on expression of genes involved in cardiac hypertrophy in fetal and adult mouse offspring

Published online by Cambridge University Press:  09 November 2010

S. Asopa ,
F. R. Cagampang ,
F. W. Anthony ,
S. A. Lanham ,
J. E. Schneider ,
S. K. Ohri  and
M. A. Hanson
S. Asopa
Affiliation:
Developmental Origins of Health and Disease Division, Institute of Developmental Sciences, University of Southampton School of Medicine, Southampton General Hospital, Southampton, UK
F. R. Cagampang*
Affiliation:
Developmental Origins of Health and Disease Division, Institute of Developmental Sciences, University of Southampton School of Medicine, Southampton General Hospital, Southampton, UK
F. W. Anthony
Affiliation:
Developmental Origins of Health and Disease Division, Institute of Developmental Sciences, University of Southampton School of Medicine, Southampton General Hospital, Southampton, UK
S. A. Lanham
Affiliation:
Developmental Origins of Health and Disease Division, Institute of Developmental Sciences, University of Southampton School of Medicine, Southampton General Hospital, Southampton, UK
J. E. Schneider
Affiliation:
Department of Cardiovascular Medicine, British Heart Foundation Molecular Cardiology Laboratory, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK
S. K. Ohri
Affiliation:
Wessex Cardiothoracic Centre, Southampton General Hospital, Southampton, UK
M. A. Hanson
Affiliation:
Developmental Origins of Health and Disease Division, Institute of Developmental Sciences, University of Southampton School of Medicine, Southampton General Hospital, Southampton, UK
*
*Address for correspondence: F. R. Cagampang, Developmental Origins of Health and Disease Division, Institute of Developmental Sciences, University of Southampton School of Medicine, Southampton General Hospital, Mailpoint 887, Southampton SO16 6YD, UK. (Email f.cagampang@soton.ac.uk)
Get access Rights & Permissions [Opens in a new window]

Abstract

Gene markers for cardiomyocyte growth, proliferation and remodeling were examined in mouse fetuses and adult male offspring exposed to maternal low-protein (LP) diet during pregnancy. Whole heart volume, measured by magnetic resonance imaging, was smaller in day 15 LP fetuses v. those from chow-fed dams (C), whereas heart volume was greater in adult LP v. C offspring. These LP offspring were hypertensive and had larger cardiomyocytes v. C animals. The mRNA levels of cyclin G1, a marker for cell growth, were lower in LP fetal hearts v. C hearts, but similar in the left ventricle of adult LP and C offspring. Opposite trends were found in brain natriuretic peptide levels (a marker of cardiac hypertrophy). Thus, maternal LP during pregnancy results in smaller fetal hearts and is accompanied by changes in expression of genes involved in cardiomyocyte growth, which are associated with cardiac hypertrophy and hypertension in adulthood.

Keywords

BNPcardiac hypertrophycell cycle regulationcyclin G1MRI
Type
Brief Report
Information
Journal of Developmental Origins of Health and Disease , Volume 1 , Issue 6 , December 2010 , pp. 371 - 375
Copyright
Copyright © Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2010

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1. Barker, DJ, Clark, PM. Fetal undernutrition and disease in later life. Rev Reprod. 1997; 2, 105–112.CrossRefGoogle ScholarPubMed
2. Fowden, AL, Giussani, DA, Forhead, AJ. Intrauterine programming of physiological systems: causes and consequences. Physiology (Bethesda). 2006; 21, 29–37.Google ScholarPubMed
3. Olson, EN, Schneider, MD. Sizing up the heart: development redux in disease. Genes Dev. 2003; 17, 1937–1956.CrossRefGoogle ScholarPubMed
4. Tarry-Adkins, JL, Martin-Gronert, MS, Chen, JH, Cripps, RL, Ozanne, SE. Maternal diet influences DNA damage, aortic telomere length, oxidative stress, and antioxidant defense capacity in rats. FASEB J. 2008; 22, 2037–2044.CrossRefGoogle ScholarPubMed
5. Clubb, FJ Jr, Bishop, SP. Formation of binucleated myocardial cells in the neonatal rat. An index for growth hypertrophy. Lab Invest. 1984; 50, 571–577.Google ScholarPubMed
6. Clubb, FJ Jr, Penney, DG, Bishop, SP. Cardiomegaly in neonatal rats exposed to 500 ppm carbon monoxide. J Mol Cell Cardiol. 1989; 21, 945–955.CrossRefGoogle ScholarPubMed
7. Corstius, HB, Zimanyi, MA, Maka, N, et al. Effect of intrauterine growth restriction on the number of cardiomyocytes in rat hearts. Pediatr Res. 2005; 57, 796–800.CrossRefGoogle ScholarPubMed
8. Nozato, T, Ito, H, Tamamori, M, et al. G1 cyclins are involved in the mechanism of cardiac myocyte hypertrophy induced by angiotensin II. Jpn Circ J. 2000; 64, 595–601.CrossRefGoogle ScholarPubMed
9. DeGregori, J, Leone, G, Ohtani, K, Miron, A, Nevins, JR. E2F-1 accumulation bypasses a G1 arrest resulting from the inhibition of G1 cyclin-dependent kinase activity. Genes Dev. 1995; 9, 2873–2887.CrossRefGoogle ScholarPubMed
10. Dyson, N. The regulation of E2F by pRB-family proteins. Genes Dev. 1998; 12, 2245–2262.CrossRefGoogle ScholarPubMed
11. Li, JM, Poolman, RA, Brooks, G. Role of G1 phase cyclins and cyclin-dependent kinases during cardiomyocyte hypertrophic growth in rats. Am J Physiol. 1998; 275, H814–H822.Google ScholarPubMed
12. Gardner, DG. Natriuretic peptides: markers or modulators of cardiac hypertrophy? Trends Endocrinol Metab. 2003; 14, 411–416.CrossRefGoogle ScholarPubMed
13. Nishikimi, T, Maeda, N, Matsuoka, H. The role of natriuretic peptides in cardioprotection. Cardiovasc Res. 2006; 69, 318–328.CrossRefGoogle ScholarPubMed
14. Krege, JH, Hodgin, JB, Hagaman, JR, Smithies, O. A noninvasive computerized tail-cuff system for measuring blood pressure in mice. Hypertension. 1995; 25, 1111–1115.CrossRefGoogle ScholarPubMed
15. Du, XJ. Gender modulates cardiac phenotype development in genetically modified mice. Cardiovasc Res. 2004; 63, 510–519.CrossRefGoogle ScholarPubMed
16. Schneider, JE, Bose, J, Bamforth, SD, et al. Identification of cardiac malformations in mice lacking Ptdsr using a novel high-throughput magnetic resonance imaging technique. BMC Dev Biol. 2004; 4, 16–27.CrossRefGoogle ScholarPubMed
17. Schneider, JE, Wiesmann, F, Lygate, CA, Neubauer, S. How to perform an accurate assessment of cardiac function in mice using high-resolution magnetic resonance imaging. J Cardiovasc Magn Reson. 2006; 8, 693–701.CrossRefGoogle ScholarPubMed
18. Hannan, RD, Stefanovsky, V, Taylor, L, Moss, T, Rothblum, LI. Overexpression of the transcription factor UBF1 is sufficient to increase ribosomal DNA transcription in neonatal cardiomyocytes: implications for cardiac hypertrophy. Proc Natl Acad Sci USA. 1996; 93, 8750–8755.CrossRefGoogle ScholarPubMed
19. Sanij, E, Poortinga, G, Sharkey, K, et al. UBF levels determine the number of active ribosomal RNA genes in mammals. J Cell Biol. 2008; 183, 1259–1274.CrossRefGoogle ScholarPubMed
20. Bicknell, KA, Coxon, CH, Brooks, G. Can the cardiomyocyte cell cycle be reprogrammed? J Mol Cell Cardiol. 2007; 42, 706–721.CrossRefGoogle ScholarPubMed
21. Campanero, MR, Armstrong, MI, Flemington, EK. CpG methylation as a mechanism for the regulation of E2F activity. Proc Natl Acad Sci USA. 2000; 97, 6481–6486.CrossRefGoogle ScholarPubMed
22. Tonkiss, J, Trzcińska, M, Galler, JR, Ruiz-Opazo, N, Herrera, VLM. Prenatal malnutrition-induced changes in blood pressure: dissociation of stress and nonstress responses using radiotelemetry. Hypertension. 1998; 32, 108–114.CrossRefGoogle ScholarPubMed
23. Tarry-Adkins, JL, Martin-Gronert, MS, Chen, JH, Cripps, RL, Ozanne, SE. Maternal diet influences DNA damage, aortic telomere length, oxidative stress, and antioxidant defense capacity in rats. FASEB J. 2008; 22, 2037–2044.CrossRefGoogle ScholarPubMed
24. Pimentel, DR, Adachi, T, Ido, Y, et al. Strain-stimulated hypertrophy in cardiac myocytes is mediated by reactive oxygen species-dependent Ras S-glutathiolation. J Mol Cell Cardiol. 2006; 41, 613–622.CrossRefGoogle ScholarPubMed
25. Rodford, JL, Torrens, C, Siow, RC, et al. Endothelial dysfunction and reduced antioxidant protection in an animal model of the developmental origins of cardiovascular disease. J Physiol. 2008; 586, 4709–4720.CrossRefGoogle Scholar