Key result
Pregnancy upregulates rat LV collagen III mRNA ~11-fold, driving dynamic extracellular matrix remodeling.
Pregnancy differentially regulates collagen types I and III in the rat heart, suggesting a molecular mechanism for regulating ventricular stiffness during pregnancy-induced volume overload.
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Rat data suggest collagen shifts may modulate cardiac stiffness in pregnancy volume overload; leaves open human relevance.
The pathologic cardiac remodeling has been widely documented; however, the physiological cardiac remodeling induced by pregnancy and its reversion in postpartum are poorly understood. In the present study we investigated the changes in collagen I (Col I) and collagen III (Col III) mRNA and protein levels in left ventricle from rat heart during pregnancy and postpartum. Col I and Col III mRNA expression in left ventricle samples during pregnancy and postpartum were analyzed by using quantitative PCR. Data obtained from gene expression show that Col I and Col III in left ventricle are upregulated during pregnancy with reversion in postpartum. In contrast to gene expression, the protein expression evaluated by western blot showed that Col I is downregulated and Col III is upregulated in left ventricle during pregnancy. In conclusion, the pregnancy differentially regulates collagens types I and III in heart; this finding could be an important molecular mechanism that regulates the ventricular stiffness in response to blood volume overload present during pregnancy which is reversed in postpartum.
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Limón-Miranda et al. (2014) studied Physiological cardiac remodeling during pregnancy and postpartum (n=40). Pregnancy and postpartum physiological remodeling vs. Nonpregnant control rats (diestrus) was evaluated on Left ventricular collagen type I and type III mRNA and protein expression (Col I mRNA 2.7-fold, Col III mRNA 10.9-fold, Col III protein 1.6-fold in late pregnancy vs nonpregnant, p=≤0.05). Pregnancy in rats upregulated left ventricular Col I (2.7-fold) and Col III (10.9-fold) mRNA at 21 days while decreasing Col I protein and increasing Col III protein (1.6-fold).
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