[Expression of gamma-aminobutyric acid type A receptor beta3 subunit in murine cleft palate induced by 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin].
Authors of this article are:
Lei JQ, Qiu L, Ding XH, Fu YX, Yuan XG, Liu Y.
A summary of the article is shown below:
in English, Chinese目的： 利用2,3,7,8-四氯二苯并二■英（2,3,7,8-tetrachlorodibenzo-p-dioxin，TCDD）诱导C57BL/6J胎鼠腭裂，检测γ-氨基丁酸A型受体β3亚基（gamma-aminobutyric acid type A receptor beta3 subunit，GABRB3）在TCDD诱导胎鼠腭裂模型中的表达变化情况，探讨腭裂的发生机制。 方法： 将60只孕鼠按随机数字表法分为实验组和对照组，每组30只。妊娠第10.5天（gestation day10.5，GD10.5）实验组以28 μg/kg的TCDD单次灌胃，对照组以5.6 ml/kg玉米油单次灌胃。分别在GD13.5、GD14.5、GD15.5、GD16.5、GD17.5处死孕鼠12只，每组处死6只。行胎鼠腭部形态学和组织学观察；应用实时荧光定量PCR和蛋白质印迹法检测胎鼠腭部组织中GABRB3 mRNA及蛋白表达；免疫组织化学及免疫荧光染色检测GABRB3蛋白的表达部位。 结果： 实验组共36只胎鼠，GD17.5腭裂的发生率为100%（36/36）；对照组共47只胎鼠，无腭裂发生（0/47）。实验组胎鼠腭突上抬在GD15.5完成，较对照组腭突上抬延迟1 d；GD14.5、GD15.5、GD16.5、GD17.5实验组中GABRB3基因mRNA（分别为0.561±0.073、0.728±0.104、0.782±0.137、0.686±0.145）和蛋白表达（分别为0.288±0.013、0.404±0.017、0.399±0.012、0.307±0.010）均显著低于对照组GABRB3基因mRNA（分别为0.818±0.088、0.865±0.086、1.021±0.054、1.163±0.179）和蛋白表达（分别为0.481±0.017、0.456±0.009、0.474±0.016、0.529±0.015）（P<0.05）；免疫组化及免疫荧光结果显示，GABRB3主要表达于腭突间质细胞和腭突中嵴上皮缝。 结论： TCDD诱导胎鼠腭突上抬延迟并最终导致腭裂发生可能与GABRB3降低有关；GABRB3可能在腭部发育的上抬和融合期发挥重要作用。.Objective: To investigate the expression of gamma-aminobutyric acid type A receptor beta3 subunit (GABRB3) on cleft palate in C57BL/6J mice induced by 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD). Methods: Sixty C57BL/6J pregnant mice on gestation day (GD) 10.5 were divided into two groups: one group was administered through gastric tubes one dose of 28 μg/kg TCDD (experimental group) and the other group was administered through gastric tubes one dose of 5.6 ml/kg corn oil (control group). Embryos were removed by cesarean section from pregnant mice during the palatal formation stage (GD 13.5-17.5) and the palatal tissue studied in morphological and histological observation. The relative mRNA and protein expression of GABRB3 was measured by real-time quantitative PCR and Western blotting. Localization of GABRB3 protein was measured by immunohistochemistry or immunofluorescence. Results: The incidence of cleft palate at GD17.5 was 100% in experimental group and there was no cleft palate occurred in the control group (0); elevation of palatine processes in experimental group was completed on GD15.5 which was clearly delayed by a day compared with that in control group. On GD14.5-GD17.5, the mRNA expression (0.561±0.073, 0.728±0.104, 0.782±0.137, 0.686±0.145) and protein expression (0.288±0.013, 0.404±0.017, 0.399±0.012, 0.307±0.010) in the experimental group were significantly lower than the control group mRNA expression (0.818±0.088, 0.865±0.086, 1.021±0.054, 1.163±0.179) and protein expression (0.481±0.017, 0.456±0.009, 0.474±0.016, 0.529±0.015)(P<0.05). Immunohistochemistry and immunofluorescence showed that GABRB3 was mainly expressed in the mesenchymal cells and medial edge epithelium. Conclusions: TCDD delayed palatal shelf elevation and eventually led to cleft palate may be associated with a decrease in GABRB3. GABRB3 may play an important role in the elevation and fusion phases of the palate development.
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This article is a good source of information and a good way to become familiar with topics such as: Cleft palate; Gamma-aminobutyric acid type A receptor beta3 subunit; Tetrachlorodibenzodioxin.
