Maternal nutrient restriction and the fetal left ventricle: Decreased angiotensin receptor expression
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BioMed Central
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Maternal nutrient restriction and the fetal left ventricle: Decreased angiotensin receptor expression Jeffrey S Gilbert1,2, Alvin L Lang2 and Mark J Nijland*1 Address: 1Center for Pregnancy and Newborn Research, Department of Obstetrics and Gynecology, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA and 2Department of Zoology and Physiology, University of Wyoming, Laramie, WY, USA Email: Jeffrey S Gilbert - [email protected]; Alvin L Lang - [email protected]; Mark J Nijland* - [email protected] * Corresponding author
Published: 14 July 2005 Reproductive Biology and Endocrinology 2005, 3:27 27
doi:10.1186/1477-7827-3-
Received: 26 May 2005 Accepted: 14 July 2005
This article is available from: http://www.rbej.com/content/3/1/27 © 2005 Gilbert et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract Background: Adequate maternal nutrition during gestation is requisite for fetal nutrition and development. While a large group of epidemiological studies indicate poor fetal nutrition increases heart disease risk and mortality in later life, little work has focused on the effects of impaired maternal nutrition on fetal heart development. We have previously shown that 50% global nutrient restriction from 28–78 days of gestation (early to mid-pregnancy; term = 147 days) in sheep at midgestation retards fetal growth while protecting growth of heart and results in hypertensive male offspring at nine months of age. In the present study, we evaluate LV gene transcription using RNA protection assay and real-time reverse transcriptase polymerase chain reaction, and protein expression using western blot, of VEGF and AT1 and AT2 receptors for AngII at mid-gestation in fetuses from pregnant ewes fed either 100% (C) or 50% (NR) diet during early to mid-gestation. Results: No difference between the NR (n = 6) and C (n = 6) groups was found in gene transcription of the AngII receptors. Immunoreactive AT1 (1918.4 +/- 154.2 vs. 3881.2 +/- 494.9; P < 0.01) and AT2 (1729.9 +/- 293.6 vs. 3043.3 +/- 373.2; P < 0.02) was decreased in the LV of NR fetuses compared to C fetuses. The LV of fetuses exposed to NR had greater transcription of mRNA for VEGF (5.42 ± 0.85 vs. 3.05 ± 0.19; P < 0.03) than respective C LV, while no change was observed in immunoreactive VEGF. Conclusion: The present study demonstrates that VEGF, AT1 and AT2 message and protein are not tightly coupled, pointing to post-transcriptional control points in the mid gestation NR fetus. The present data also suggest that the role of VEGF and the renin-angiotensin system receptors during conditions inducing protected cardiac growth is distinct from the role these proteins may play in normal fetal cardiac growth. The present findings may help explain ep
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