中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2012年
42期
7897-7900
,共4页
王莎%宋容%王利婷%张瑞%司庆宗%王建林%赵望泓
王莎%宋容%王利婷%張瑞%司慶宗%王建林%趙望泓
왕사%송용%왕리정%장서%사경종%왕건림%조망홍
全反式维甲酸%Smad2/3%腭裂%小鼠%免疫组织化学
全反式維甲痠%Smad2/3%腭裂%小鼠%免疫組織化學
전반식유갑산%Smad2/3%악렬%소서%면역조직화학
背景:部分学者通过体外器官培养研究认为全反式维甲酸干扰了Smad2/3在腭部的表达,具体机制尚不明确.目的:观察腭突Smad2/3信号分子在胚鼠腭部发育及腭裂形成过程中的表达变化.方法:54只C57BL/6J近交系孕鼠随机分为3组,在妊娠10 d,实验组一次性灌胃全反式维甲酸100 mg/kg诱导胚鼠两侧腭突不能在中线融合,建立腭裂畸形动物模型;植物油对照组灌胃10 mL/kg橄榄油,空白对照组不做处理.结果与结论:在植物油对照组中,从妊娠13 d 18时到妊娠14 d 18时腭间充质细胞中Smad2/3免疫阳性表达逐步增高,至妊娠15 d 8时表达开始出现下降,实验组也表现为这一变化趋势,且同一组间表达较植物油对照组明显;在腭中嵴上皮细胞中,植物油对照组随着腭突的融合,腭中嵴上皮带消失,Smad2/3表达也明显下降,实验组始终未融合,未见明显的Smad2/3阳性细胞.在整个胚腭正常发育和腭裂形成过程中,空白对照组与植物油对照组Smad2/3阳性细胞表达几乎无差异.提示过量全反式维甲酸可能通过干扰腭中嵴上皮细胞及间充质细胞中Smad2/3信号分子的表达,从而影响小鼠胚腭上皮间充质转化,与腭裂形成密切相关.
揹景:部分學者通過體外器官培養研究認為全反式維甲痠榦擾瞭Smad2/3在腭部的錶達,具體機製尚不明確.目的:觀察腭突Smad2/3信號分子在胚鼠腭部髮育及腭裂形成過程中的錶達變化.方法:54隻C57BL/6J近交繫孕鼠隨機分為3組,在妊娠10 d,實驗組一次性灌胃全反式維甲痠100 mg/kg誘導胚鼠兩側腭突不能在中線融閤,建立腭裂畸形動物模型;植物油對照組灌胃10 mL/kg橄欖油,空白對照組不做處理.結果與結論:在植物油對照組中,從妊娠13 d 18時到妊娠14 d 18時腭間充質細胞中Smad2/3免疫暘性錶達逐步增高,至妊娠15 d 8時錶達開始齣現下降,實驗組也錶現為這一變化趨勢,且同一組間錶達較植物油對照組明顯;在腭中嵴上皮細胞中,植物油對照組隨著腭突的融閤,腭中嵴上皮帶消失,Smad2/3錶達也明顯下降,實驗組始終未融閤,未見明顯的Smad2/3暘性細胞.在整箇胚腭正常髮育和腭裂形成過程中,空白對照組與植物油對照組Smad2/3暘性細胞錶達幾乎無差異.提示過量全反式維甲痠可能通過榦擾腭中嵴上皮細胞及間充質細胞中Smad2/3信號分子的錶達,從而影響小鼠胚腭上皮間充質轉化,與腭裂形成密切相關.
배경:부분학자통과체외기관배양연구인위전반식유갑산간우료Smad2/3재악부적표체,구체궤제상불명학.목적:관찰악돌Smad2/3신호분자재배서악부발육급악렬형성과정중적표체변화.방법:54지C57BL/6J근교계잉서수궤분위3조,재임신10 d,실험조일차성관위전반식유갑산100 mg/kg유도배서량측악돌불능재중선융합,건립악렬기형동물모형;식물유대조조관위10 mL/kg감람유,공백대조조불주처리.결과여결론:재식물유대조조중,종임신13 d 18시도임신14 d 18시악간충질세포중Smad2/3면역양성표체축보증고,지임신15 d 8시표체개시출현하강,실험조야표현위저일변화추세,차동일조간표체교식물유대조조명현;재악중척상피세포중,식물유대조조수착악돌적융합,악중척상피대소실,Smad2/3표체야명현하강,실험조시종미융합,미견명현적Smad2/3양성세포.재정개배악정상발육화악렬형성과정중,공백대조조여식물유대조조Smad2/3양성세포표체궤호무차이.제시과량전반식유갑산가능통과간우악중척상피세포급간충질세포중Smad2/3신호분자적표체,종이영향소서배악상피간충질전화,여악렬형성밀절상관.
BACKGROUND:Through in vitro organ culture studies, a few scholars consider that al-trans retinoic acid (at RA) can interfere with palatal expression, but the underlying mechanisms remain unclear. OBJECTIVE:To investigate the expression changes of Smad2/3 of palatal shelves in normal palatal development and cleft palate formation during mouse embryogenesis. METHODS:Both sides of the embryonic mouse palatal shelves were induced by excess at RA so that they could not integrate at the midline. Then, a mouse model of cleft palate was established, and 54 C57BL/6J inbred pregnant mice were randomly divided into experimental group, vegetable oil control group and blank control group. At GD 10, the mice in the experimental group were subjected to once gastric perfusion with 100 mg/kg at RA, and those in the vegetable o control group underwent lavage with 10mL/kg olive oil, while those in the blank control group had no treatment. RESULTS AND CONCLUSION:Smad2/3 positive expression was increased gradual y in the embryonic palatal mesenchymal cel s from GD1318 to GD148, but few positive cel s were observed after GD158, while this trend was also found in the experimental group. In addition, Smad2/3 positive expression at the same developmental time was more obvious than that of the vegetable oil control group. In palatal medial edge epithelium, with the integration of bilateral palatal shelves, the ridge in palate belt disappeared, and Smad2/3 expression was decreased significantly. In the experimental group,the integration did not appeared, besides, significant Smad2/3 positive cel s were not found. There was no significant difference in Smad2/3 positive cel expression between the blank control and vegetable oil groups in normal palatal development and cleft palate formation during mouse embryogenesis. These results suggest that excess at RA can interfere with Smad2/3 expression in the embryonic palatal medial edge epithelium and embryonic palatal mesenchymal cel s, and thereby influence epithelial-mesenchymal transformation in mice, which is closely related to the formation of cleft palate.