Mechanism of cleft palate in C57BL/6N mice induced by retinoic acid
10.3760/cma.j.issn.1002-0098.2017.11.008
- VernacularTitle: 全反式维甲酸诱导小鼠腭裂作用机制初探
- Author:
Xiaozhuan LIU
1
;
Yuchang TAO
2
;
Xiuli ZHANG
2
;
Zengli YU
2
Author Information
1. Department of Scientific Research and Discipline Construction, Henan Provincial People's Hospital, Zhengzhou 450000, China
2. Public Health College, Zhengzhou University, Zhengzhou 450001, China
- Publication Type:Journal Article
- Keywords:
Tretinoin;
Cleft palate;
Smad proteins
- From:
Chinese Journal of Stomatology
2017;52(11):690-694
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the mechanism of cleft palate in mice induced by excessive all-trans retinoic acid (atRA).
Methods:The pregnant mice were randomly divided into atRA-treated group (n=27) and control group (n=27). atRA-treated group was given by gavage a single dose of atRA (100 mg/kg) at 8: 00 AM on gestation day 10 (GD10) and the control group was given by gavage the isopyknic corn oil. At GD13-GD15, the fetal mice palate development was observed by HE staining. The mouse embryonic palatal mesenchymal cell proliferation was detected by 5-bromo-2-deoxyuridine (BrdU) immunohistochemistry. The expressions of Smad2, phospho-Smad2 (p-Smad2), Smad4 and Smad7 in mouse embryonic palatal mesenchyme were analyzed by Western blotting.
Results:At GD13-GD15, compared with the control, the ratio of BrdU-positive cells in the palatal mesenchyme of atRA-treated fetuses decreased significantly (P<0.05), especially at GD14, atRA inhibition rate was (65.4±1.7)%. Moreover, atRA decreased the levels of p-Smad2 and Smad4 in embryonic palate mesenchymal cells, whereas the expression of Smad7 was significantly increased at GD14 and GD15.
Conclusions:atRA may lead to cleft palate by inhibiting the activation of Smad signaling pathway and affecting the proliferation of palatal mesenchymal cells.
