Molecular mechanism of cleft palate induced by retinoic acid

• Published in: Wei sheng yan jiu Vol. 33; no. 6; p. 690
• Main Authors: Zhu, Jiangbo, Yin, Muquan, Zhu, Yuping, Chen, Rongfang, Wan, Xuying, Ma, Xili, Guo, Miaoli, Zhang, Tianbao
• Format: Journal Article
• Language: Chinese
• Published: China 01.11.2004
• Subjects: Animals; Apoptosis; Cleft Palate - chemically induced; Cleft Palate - genetics; Cleft Palate - pathology; Down-Regulation; Female; Gene Expression Profiling; Gene Expression Regulation, Developmental; Glypicans; Heparan Sulfate Proteoglycans - genetics; Male; Membrane Proteins - genetics; Mice; Mice, Inbred ICR; Nucleic Acid Hybridization; Tenascin - genetics; Tretinoin - toxicity; Up-Regulation
• ISSN: 1000-8020

To explore the molecular mechanism of cleft palate induced by chemicals. Retinoic acid was used as a known teratogen to induce cleft palate in ICR mice and a suppression subtractive hybridization (SSH) technique was applied to identify differentially expressed genes that related to cleft palate of ICR mice. 14 reverse differently and 9 forward differentially expressed clones were obtained. Some clones were selected to be sequenced and aligned to GenBank. In this study, suppressed Gpc3 and Insulin-Induced protein 1 could affect growth of palate shelves and resulted in cleft palate by reducing the size of the palate shelves. Down-regulation of Ptprs interfered with a cell signal pathway and down-regulation of Tn C inhibited the cell de-adhesion and expression of Egfr, then suppressed Egfr prevented the normal expression of MMPs that influenced the medial edge epithelium disruption and caused cleft palate. Tn C could bind to Ptprs and Gpcs, and HSPGs were ligands for Ptrps. Up-regulate of Rps25 might play a role