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High Salt Induces Developmental Defect during Pregnancy
Author(s) -
Yen ChingTzu,
Pai ChenHsueh,
Hong ChiaLun,
Chang ShengKai,
Yu IShing,
Lin ShuRung,
Lin ShuWha
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.767.4
Subject(s) - fetus , pregnancy , placenta , medicine , endocrinology , thromboxane b2 , thromboxane a2 , biology , andrology , physiology , receptor , genetics , platelet
With the process of civilization, daily diet in our lives are filled with high salt, fat and carbohydrate foods, and the onset ages of high blood pressure, diabetes, and cardiovascular disease are getting younger. Increase in the diet burden also leads to higher risk for pregnant women and childbirth and may even affect embryo's growth. This study is to investigate the effect of high salt intake on the development of placentas and fetus during pregnancy. We treated pregnant mice with high salt drinking water as a model. Our results revealed that high salt induced elevation of blood pressure and severe decrease of maternal body weight, fetal size and fetal weight in mice during pregnancy. Placentas of high salt drinking water‐treated pregnant mice showed loosely organized features, aberrantly distributed spongiotrophoblast, less‐vascularized labyrinth zone, increased cellular apoptosis, and suppressed cellular proliferation. Furthermore, high salt induced an increase of the Thromboxane A 2 Synthase (TXAS) and the increased expression of the p27. This indicated that high salt may limits the differentiation and enhances apoptosis of placental trophoblasts through up‐regulation of Thromboxane A2 and p27. In line with this finding, we found that the TXAS knockout mice were more resistant to high salt treatment, implying a role of TXA 2 on the development of maternal and fetal defects during high salt treatment. Taken together, this study indicated that high salt affects the development of placenta that might result in insufficient materials‐fetal exchanges and lead to deteriorate growth defects of fetus.