Cigarette smoke induced neural tube defects by down‐regulating noggin expression. Issue 1 (19th September 2020)

• Record Type: Journal Article
• Authors: Yin, Chuanhui; Cai, Heng; Yang, Dandan; Jian, Yi; Zhang, Jinfeng; Li, Zhiwen; Wang, Dong
• Is Part Of: Birth defects research. Volume 113:Issue 1(2021)
• Page Start: 5
• Page End: 13
• Publication Date: 2020-09-19
• Subjects: BMP2 -- cigarette smoke -- neural tube defects -- noggin; Teratology -- Periodicals; Abnormalities, Human -- Periodicals; Congenital Abnormalities; Embryo, Mammalian -- abnormalities; Teratology; Abnormalities, Human; Teratology; Periodicals; Periodicals; 616.043
• DOI: 10.1002/bdr2.1804
• Languages: English
• ISSNs: 2472-1727

Abstract

Abstract: Background: Maternal smoking or passive smoking during gestation increases the risk of congenital birth defects, including neural tube defects (NTDs). Cigarette smoke is a recognized teratogen that causes NTDs, although the mechanisms are not well understood. Methods: An established model of passive smoking in pregnant golden hamsters was used to observe the effect of cigarette smoke on neural tube development using scanning electron microscopy. Level of noggin expression in placenta and neural tube was evaluated by immunohistochemistry. Results: Our results indicated that cigarette smoke can cause the neural tube closure of the golden hamster embryo to be delayed or not closed. In normal placental tissues noggin protein and RNA levels were highly expressed, and the expression level in the term placenta was lower than in that of the first trimester or second trimester through analyzing the Human Protein Atlas and the Gene Expression Omnibus (GEO) databases. Cigarette smoke can down‐regulate noggin expression in the placenta and promote cell apoptosis. We observed that noggin expression was reduced and BMP2 expression was increased by cigarette smoke. Conclusions: Cigarette smoke may cause cell apoptosis and accelerate placenta maturation. Meanwhile, cigarette smoke may inhibit the development of the embryo, and lead to the formation of NTDs via downregulating the expression of noggin and dis‐inhibition of BMP2.