Novel insights into a retinoic-acid-induced cleft palate based on Rac1 regulation of the fibronectin arrangement

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• 作者：Qinghuang Tang ; Liwen Li ; Min-Jung Lee ; Qing Ge ; Jong-Min Lee…
• 关键词：Retinoic acid ; Rac1 ; Fibronectin ; Palatal shelf elevation ; Cleft palate ; Mouse
• 刊名：Cell and Tissue Research
• 出版年：2016
• 出版时间：March 2016
• 年：2016
• 卷：363
• 期：3
• 页码：713-722
• 全文大小：16,236 KB
• 参考文献：Abbott BD, Pratt RM (1991) Retinoic acid alters epithelial differentiation during palatogenesis. J Craniofac Genet Dev Biol 11:315–325PubMed
  Abbott BD, Harris MW, Birnbaum LS (1989) Etiology of retinoic acid-induced cleft palate varies with the embryonic stage. Teratology 40:533–553CrossRef PubMed
  Almaidhan A, Cesario J, Landin Malt A, Zhao Y, Sharma N, Choi V, Jeong J (2014) Neural crest-specific deletion of Ldb1 leads to cleft secondary palate with impaired palatal shelf elevation. BMC Dev Biol 14:3PubMedCentral CrossRef PubMed
  Brinkley LL, Bookstein FL (1986) Cell distribution during mouse secondary palate closure. II. Mesenchymal cells. J Embryol Exp Morphol 96:111–130PubMed
  Chauhan BK, Lou M, Zheng Y, Lang RA (2011) Balanced Rac1 and RhoA activities regulate cell shape and drive invagination morphogenesis in epithelia. Proc Natl Acad Sci U S A 108:18289–18294PubMedCentral CrossRef PubMed
  Clagett-Dame M, Knutson D (2011) Vitamin A in reproduction and development. Nutrients 3:385–428PubMedCentral CrossRef PubMed
  Cong W, Liu B, Liu S, Sun M, Liu H, Yang Y, Wang R, Xiao J (2014) Implications of the Wnt5a/CaMKII pathway in retinoic acid-induced myogenic tongue abnormalities of developing mice. Sci Rep 4:6082PubMedCentral CrossRef PubMed
  Cuervo R, Valencia C, Chandraratna RA, Covarrubias L (2002) Programmed cell death is required for palate shelf fusion and is regulated by retinoic acid. Dev Biol 245:145–156CrossRef PubMed
  Degitz SJ, Morris D, Foley GL, Francis BM (1998) Role of TGF-beta in RA-induced cleft palate in CD-1 mice. Teratology 58:197–204CrossRef PubMed
  Ferguson MW (1988) Palate development. Development 103 (Suppl):41–60PubMed
  Gritli-Linde A (2007) Molecular control of secondary palate development. Dev Biol 301:309–326CrossRef PubMed
  Gritli-Linde A (2008) The etiopathogenesis of cleft lip and cleft palate: usefulness and caveats of mouse models. Curr Top Dev Biol 84:37–138CrossRef PubMed
  He F, Popkie AP, Xiong W, Li L, Wang Y, Phiel CJ, Chen Y (2010) Gsk3beta is required in the epithelium for palatal elevation in mice. Dev Dyn 239:3235–3246PubMedCentral CrossRef PubMed
  Horie S, Yasuda M (2001) Alterations in palatal ruga patterns in Jcl:ICR mouse fetuses from dams treated with all-trans-retinoic acid. Hiroshima J Med Sci 50:17–25PubMed
  Hu X, Gao J, Liao Y, Tang S, Lu F (2013) Retinoic acid alters the proliferation and survival of the epithelium and mesenchyme and suppresses Wnt/beta-catenin signaling in developing cleft palate. Cell Death Dis 4:e898PubMedCentral CrossRef PubMed
  Ines FM, Valeria GG, Lis SM, Silvina NB, Matias SA, Maria VR (2014) Retinoic acid reduces migration of human breast cancer cells: role of retinoic acid receptor beta. J Cell Mol Med 18:1113–1123CrossRef
  Liang CC, Park AY, Guan JL (2007) In vitro scratch assay: a convenient and inexpensive method for analysis of cell migration in vitro. Nat Protoc 2:329–333CrossRef PubMed
  Okano J, Suzuki S, Shiota K (2007) Involvement of apoptotic cell death and cell cycle perturbation in retinoic acid-induced cleft palate in mice. Toxicol Appl Pharmacol 221:42–56CrossRef PubMed
  Pratt RM, Goulding EH, Abbott BD (1987) Retinoic acid inhibits migration of cranial neural crest cells in the cultured mouse embryo. J Craniofac Genet Dev Biol 7:205–217PubMed
  Sohn WJ, Yamamoto H, Shin HI, Ryoo ZY, Lee S, Bae YC, Jung HS, Kim JY (2011) Importance of region-specific epithelial rearrangements in mouse rugae development. Cell Tissue Res 344:271–277CrossRef PubMed
  Suwa F, Jin Y, Lu H, Li X, Tipoe GL, Lau TY, Tamada Y, Kuroki K, Fang YR (2001) Alteration of apoptosis in cleft palate formation and ectomesenchymal stem cells influenced by retinoic acid. Okajimas Folia Anat Jpn 78:179–186CrossRef PubMed
  Tang Q, Li L, Jin C, Lee JM, Jung HS (2015) Role of region-distinctive expression of Rac1 in regulating fibronectin arrangement during palatal shelf elevation. Cell Tissue Res (in press)
  Tsunekawa N, Arata A, Obata K (2005) Development of spontaneous mouth/tongue movement and related neural activity, and their repression in fetal mice lacking glutamate decarboxylase 67. Eur J Neurosci 21:173–178CrossRef PubMed
  Wang W, Kirsch T (2002) Retinoic acid stimulates annexin-mediated growth plate chondrocyte mineralization. J Cell Biol 157:1061–1069PubMedCentral CrossRef PubMed
  Xiao WL, Shi B, Huang L, Zheng Q, Li S, Lu Y (2006) Separation and culture of mouse embryonic palatal mesenchymal cells in vitro. Sichuan Da Xue Xue Bao Yi Xue Ban 37:137–140PubMed
  
• 作者单位：Qinghuang Tang (1)
  Liwen Li (1)
  Min-Jung Lee (1)
  Qing Ge (1)
  Jong-Min Lee (1)
  Han-Sung Jung (1) (2)
  
  1. Division in Anatomy and Developmental Biology, Department of Oral Biology, Oral Science Research Center, BK21 PLUS Project, Yonsei University College of Dentistry, Seoul, Korea
  2. Oral Biosciences, Faculty of Dentistry, The University of Hong Kong, Hong Kong, SAR, People’s Republic of China
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Human Genetics
  Proteomics
  Molecular Medicine
  
• 出版者：Springer Berlin / Heidelberg
• ISSN：1432-0878

文摘

Retinoic acid (RA)-induced cleft palate results from both extrinsic obstructions by the tongue and internal factors within the palatal shelves. Our previous study showed that the spatiotemporal expression of Rac1 regulates the fibronectin (FN) arrangement through cell density alterations that play an important role in palate development. In this study, we investigate the involvement of the Rac1 regulation of the FN arrangement in RA-induced cleft palate. Our results demonstrate that RA-induced intrinsic alterations in palatal shelves, including a delayed progress of cell condensation, delay palate development, even after the removal of the tongue. Further analysis shows that RA treatment diminishes the region-distinctive expression of Rac1 within the palatal shelves, which reversely alters the fibrillar arrangement of FN. Furthermore, RA treatment disrupts the formation of lamellipodia, which are indicative structures of cell migration that are regulated by Rac1. These results suggest that the Rac1 regulation of the FN arrangement is involved in RA-induced cleft palate through the regulation of cell migration, which delays the progress of cell condensation and subsequently influences the FN arrangement, inducing a delay in palate development. Our study provides new insights into the RA-induced impairment of palatal shelf elevation based on cell migration dynamics.