Pregnancy-induced changes in renin gene expression in mice

Area of Science:

• Reproductive biology
• Endocrinology
• Physiology

Background:

• The renin-angiotensin system (RAS) shows significant, yet poorly understood, alterations during pregnancy, including elevated maternal circulating prorenin and renin.
• The physiological significance of these pregnancy-induced changes in RAS components remains unclear.

Purpose of the Study:

• To establish and utilize a murine model to investigate the changes in renin-angiotensin system components during pregnancy.
• To identify the specific maternal tissues and genes responsible for increased renin production during gestation.

Main Methods:

• Utilized pregnant ICR mice (Ren1 and Ren2 genes) and C57Bl/6 mice (Ren1 gene only) to study renin gene expression.
• Analyzed renin protein levels in maternal circulation.
• Examined renin gene expression in maternal decidua, placenta, and kidneys.

Main Results:

• Pregnant mice exhibit increased circulating renin protein, validating the mouse as a model for pregnancy-related RAS changes.
• In ICR mice, renin gene expression is upregulated in the maternal decidua and placenta.
• In C57Bl/6 mice, pregnancy-induced renin gene expression is primarily observed in the kidneys, with minimal placental expression.

Conclusions:

• Mice serve as a valuable and convenient model for studying pregnancy-induced alterations in the renin-angiotensin system.
• Gestation-induced renin gene expression occurs at the mother-fetus interface, particularly in the decidua and placenta, though the specific sites can vary depending on the mouse strain and renin gene repertoire.
• These findings highlight the complexity of RAS regulation during pregnancy and offer insights into tissue-specific gene expression patterns.