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Published on: November 22, 2013
The earliest impact of restricted protein intake during pregnancy on heart development in male mouse offspring
Marina S Folguieri1, Bruno Calsa1, Patricia Aline Boer1
1Fetal Programming and Hydroelectrolyte Metabolism Laboratory, Department of Internal Medicine, Nucleus of Medicine and Experimental Surgery, FCM, Campinas, Brazil.
Insights
Maternal protein restriction during pregnancy increases apoptosis markers in offspring hearts, potentially leading to cardiac remodeling and fibrosis. Autophagy remained unchanged, suggesting specific cellular pathways are affected by nutritional deprivation.
Area of Science:
- Developmental Biology
- Nutritional Science
- Cardiovascular Research
Background:
- Maternal protein restriction in animal models is linked to adverse outcomes like reduced birth weight and hypertension.
- Gestational protein deficiency affects cardiac mass, fibroblast presence, and fibrosis in adult rodent ventricles.
- Nutritional deprivation may impair cellular proliferation, leading to decreased cell populations.
Purpose of the Study:
- To investigate the impact of maternal protein restriction on offspring cardiogenesis.
- To elucidate relationships between growth factor signaling, gene expression, and cardiac development under nutritional stress.
- To analyze early cardiac remodeling and cellular pathways in response to maternal dietary changes.
Main Methods:
- Analysis of female mice subjected to protein deficiency and their offspring.
- Assessment of early cardiac remodeling and key cellular pathways, including apoptosis (cleaved caspase-3) and autophagy.
- Utilized RT-qPCR, immunohistochemistry, and a transgenic model for autophagic flux quantification.
Main Results:
- Gestational protein restriction altered gene expression profiles related to cardiac remodeling.
- Increased levels of apoptotic markers were observed in offspring exposed to protein deficiency.
- No significant alterations in autophagic flux were detected.
Conclusions:
- Early protein restriction initiates cardiac remodeling, including transient heart volume expansion and cardiomyocyte hypertrophy.
- This remodeling process may progress to fibrosis and metabolic stress.
- Autophagic flux was not significantly altered, indicating specific molecular responses to nutritional insult.
Introduction:
Maternal protein restriction in animal models poses significant risks that lead to detrimental outcomes such as decreased birth weights, reduced nephron counts, neurological disorders, and increased arterial hypertension. Previous studies have shown that gestational protein deficiency is linked to reductions in cardiac mass, an increased presence of cardiac fibroblasts, and the development of fibrosis in both the left and right ventricles of adult rodents. This leads to the hypothesis that nutritional deprivation negatively impacts cellular proliferation mechanisms, ultimately resulting in a decrease in cell populations.
Aims:
The present study aims to elucidate the complex relationships among growth factor signaling, molecular expression profiles, and developmental pathways that underpin cardiac morphogenesis during the embryonic and fetal stages of development. We focus on the potentially harmful effects of maternal protein restriction on the cardiogenesis of the offspring.
Methods:
Methodologically, we analyzed the responses of female mice subjected to protein deficiency and evaluated the effects on their offspring, with a particular emphasis on early cardiac remodeling and key cellular pathways. Specifically, we analyzed cleaved caspase-3 as a marker for apoptosis, along with autophagy. Techniques employed include RT-qPCR, immunohistochemistry, and a transgenic model for direct quantification of autophagic flux.
Results:
Our findings indicate that gestational protein restriction alters the expression profiles of genes associated with cardiac remodeling and increases the levels of apoptotic markers. In contrast, autophagic flux did not show significant alterations.
Conclusion:
We conclude that early protein restriction triggers a cascade of remodeling responses, including transient heart volume expansion accompanied by cardiomyocyte hypertrophy, which may progress towards fibrosis and metabolic stress. Autophagic flux was not significantly altered. We conclude that early protein restriction triggers a cascade of remodeling responses, including a transient heart volume expansion accompanied by cardiomyocyte hypertrophy, which has the potential to progress towards fibrosis and metabolic stress.
