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Secondary Palate (secondary + palate)
Selected AbstractsRegional heterogeneity in the developing palate: morphological and molecular evidence for normal and abnormal palatogenesisCONGENITAL ANOMALIES, Issue 2 2006Junko Okano ABSTRACT Development of the mammalian secondary palate involves the growth, elevation, medial elongation and midline fusion of palatal shelves. Recent morphological and molecular studies on palatogenesis suggest that the developing palate is not a homogeneous organ but each part may behave differently during organogenesis. Especially, some key molecules involved in palate development have been shown to exhibit heterogeneous patterns of expression in the palatal tissue. Therefore it seems necessary to recognize the regional heterogeneity of the developing palate along the dorsoventral and anteroposterior axes when analyzing the mechanisms of normal and abnormal morphogenesis. Based on recent studies, we discuss the issue of the regional heterogeneity in the fetal palate and propose a principle that divides the fetal palate into several regions from the morphological and molecular standpoint. [source] Mesenchymal cell remodeling during mouse secondary palate reorientationDEVELOPMENTAL DYNAMICS, Issue 7 2010Jiu-Zhen Jin Abstract The formation of mammalian secondary palate requires a series of developmental events such as growth, elevation, and fusion. Despite recent advances in the field of palate development, the process of palate elevation remains poorly understood. The current consensus on palate elevation is that the distal end of the vertical palatal shelf corresponds to the medial edge of the elevated horizontal palatal shelf. We provide evidence suggesting that the prospective medial edge of the vertical palate is located toward the interior side (the side adjacent to the tongue), instead of the distal end, of the vertical palatal shelf and that the horizontal palatal axis is generated through palatal outgrowth from the side of the vertical palatal shelf rather than rotating the pre-existing vertical axis orthogonally. Because palate elevation represents a classic example of embryonic tissue re-orientation, our findings here may also shed light on the process of tissue re-orientation in general. Developmental Dynamics 239:2110,2117, 2010. © 2010 Wiley-Liss, Inc. [source] Analysis of Meox - 2 mutant mice reveals a novel postfusion-based cleft palateDEVELOPMENTAL DYNAMICS, Issue 2 2006Jiu-Zhen Jin Abstract Cleft palate represents a common human congential disease involving defects in the development of the secondary palate. Major steps in mammalian palatogenesis include vertical growth, elevation, and fusion of the palate shelves. Our current study with the homeobox gene Meox - 2 during mouse secondary palate development reveals a novel postfusion-based mechanism for cleft palate. Meox - 1 and Meox - 2 are two functionally related homeobox genes playing important roles in somitogenesis and limb muscle differentiation. We found that the expression of Meox - 2, not Meox - 1, marks the specification of early mouse palatal mesenchymal cells in the maxillary processes at embryonic day 11.5 (E11.5). From E12.5 to E15.5, the expression of Meox - 2 occupies only the posterior part of the palate, providing an early molecular marker for the anterior,posterior polarity in mouse secondary palate formation. A total of 35.3% of Meox - 2,/, (n = 17) and 25.5% of Meox - 2+/, (n = 55) mouse embryos display a cleft palate phenotype at E15.5, indicating that the reduction of Meox - 2 function is associated with susceptibility to cleft palate. Unlike previously reported clefts, none of the clefts found in Meox - 2 mutants contain any epithelial sheets in the medial edge areas, and detailed examination revealed that the clefts resulted from the breakdown of newly fused palates. This article is the first report of a gene required to maintain adherence of the palatal shelves after fusion. Developmental Dynamics 235:539,546, 2006. © 2005 Wiley-Liss, Inc. [source] Developmental changes in cellular and extracellular structural macromolecules in the secondary palate and in the nasal cavity of the mouseEUROPEAN JOURNAL OF ORAL SCIENCES, Issue 3 2010Forugh Vaziri Sani Vaziri Sani F, Kaartinen V, El Shahawy M, Linde A, Gritli-Linde A. Developmental changes in cellular and extracellular structural macromolecules in the secondary palate and nasal cavity of the mouse. Eur J Oral Sci 2010; 118: 221,236. © 2010 The Authors. Journal compilation© 2010 Eur J Oral Sci The aim of this study was to analyse the hitherto largely unknown expression patterns of some specific cellular and extracellular molecules during palate and nasal cavity development. We showed that epithelia of the developing palate and the vomerine epithelium express similar sets of structural proteins. With the exception of keratin 15, which becomes barely detectable in the elevated palatal shelves, nearly all of these proteins become upregulated at the presumptive areas of fusion and in the adhering epithelia of the palate and nasal septum. In vivo and in vitro analyses indicated that reduction in the amount of keratin 15 protein is independent of Tgf,,Alk5 signalling. Foxa1 expression also highlighted the regionalization of the palatal and nasal epithelia. Owing to the lack of reliable markers of the palatal periderm, the fate of peridermal cells has been controversial. We identified LewisX/stage-specific embryonic antigen-1 as a specific peridermal marker, and showed that numerous peridermal cells remain trapped in the medial epithelial seam (MES). The fate of these cells is probably apoptosis together with the rest of the MES cells, as we provided strong evidence for this event. Heparan sulphate, chondroitin-6-sulphate, and versican displayed dynamically changing distribution patterns. The hitherto-unknown innervation pattern of the developing palate was revealed. These findings may be of value for unravelling the pathogenesis of palatal clefting. [source] Intracellular dynamics of Smad-mediated TGF, signalingJOURNAL OF CELLULAR PHYSIOLOGY, Issue 2 2003Robert M. Greene The transforming growth factor-, (TGF,) family represents a class of signaling molecules that plays a central role in morphogenesis, growth, and cell differentiation during normal embryonic development. Members of this growth factor family are particularly vital to development of the mammalian secondary palate where they regulate palate mesenchymal cell proliferation and extracellular matrix synthesis. Such regulation is particularly critical since perturbation of either cellular process results in a cleft of the palate. While the cellular and phenotypic effects of TGF, on embryonic craniofacial tissue have been extensively catalogued, the specific genes that function as downstream mediators of TGF, action in the embryo during palatal ontogenesis are poorly defined. Embryonic palatal tissue in vivo and murine embryonic palate mesenchymal (MEPM) cells in vitro secrete and respond to TGF,. In the current study, elements of the Smad component of the TGF, intracellular signaling system were identified and characterized in cells of the embryonic palate and functional activation of the Smad pathway by TGF,1, TGF,2, and TGF,3 was demonstrated. TGF,-initiated Smad signaling in cells of the embryonic palate was found to result in: (1) phosphorylation of Smad 2; (2) nuclear translocation of the Smads 2, 3, and 4 protein complex; (3) binding of Smads 3 and 4 to a consensus Smad binding element (SBE) oligonucleotide; (4) transactivation of transfected reporter constructs, containing TGF,-inducible Smad response elements; and (4) increased expression of gelatinases A and B (endogenous genes containing Smad response elements) whose expression is critical to matrix remodeling during palatal ontogenesis. Collectively, these data point to the presence of a functional Smad-mediated TGF, signaling system in cells of the developing murine palate. J. Cell. Physiol. 197: 261,271, 2003. © 2003 Wiley-Liss, Inc. [source] Altered binding of MYF-5 to FOXE1 promoter in non-syndromic and CHARGE-associated cleft palateJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 1 2009Mario Venza Background:, Three different homozygous loss-of-function mutations of the Forkhead box E1 (FOXE1) gene have been associated with syndromic cleft palate. Here, we screened the entire promoter region to identify the variations in significant consensus motifs affecting FOXE1 transcription. Method:, Genomic DNAs of 35 cleft palate patients, 10 of whom with CHARGE association, 80 unrelated healthy people and 80 unaffected first-degree relatives were analysed by automatic sequencing. The Transcription Element Search System program was employed to identify transcription factor binding sites. The protein-DNA complexes were observed using DNA band-shift assays and oligonucleotide competition analyses. Real-time PCR was used to estimate FOXE1 expression at mRNA level. Results:, In 11 non-syndromic cleft palate patients, a novel non-coding polymorphism (C,G) in the 5,-untranslated region of FOXE1 was found. The variation fell into a putative consensus sequence for the transcription factor MYF-5 and completely impaired the ability of MYF -5 to bind to its motif, as shown by EMSA experiments. As a consequence, a significantly reduced FOXE1 mRNA expression was observed. Conclusions:, In 45% of non-syndromic cleft palate patients, a novel homozygous polymorphism that prevented the binding of MYF -5 to FOXE1 promoter and affected the FOXE1 expression was found. As recent data show the role of MYF-5 in the muscle-dependent craniofacial skeletal development and in the fusion of primary palate and secondary palate, the results reported here strongly suggest a more significant involvement of this factor in the cleft palate onset. [source] The internal cranial anatomy of the Plesiosauria (Reptilia, Sauropterygia): evidence for a functional secondary palateLETHAIA, Issue 4 2006Marie-Céline Buchy In the late 19th Century, the choanae (or internal nares) of the Plesiosauria were identified as a pair of palatal openings located rostral to the external nares, implying a rostrally directed respiratory duct and air path inside the rostrum. Despite obvious functional shortcomings, this idea was firmly established in the scientific literature by the first decade of the 20th Century. The functional consequences of this morphology were only re-examined by the end of the 20th Century, leading to the conclusion that the choanae were not involved in respiration but instead in underwater olfaction, the animals supposedly breathing with the mouth agape. Re-evaluation of the palatal and internal cranial anatomy of the Plesiosauria reveals that the traditional identification of the choanae as a pair of fenestrae situated rostral to the external nares appears erroneous. These openings more likely represent the bony apertures of ducts that lead to internal salt glands situated inside the maxillary rostrum. The ,real' functional choanae (or caudal interpterygoid vacuities), are situated at the caudal end of the bony palate between the sub-temporal fossae, as was suggested in the mid-19th Century. The existence of a functional secondary palate in the Plesiosauria is therefore strongly supported, and the anatomical, physiological, and evolutionary implications of such a structure are discussed. [source] Molecular fingerprinting of TGFß-treated embryonic maxillary mesenchymal cellsORTHODONTICS & CRANIOFACIAL RESEARCH, Issue 4 2003M.M. Pisano Abstract The transforming growth factor-ß (TGFß) family represents a class of signaling molecules that plays a central role in normal embryonic development, specifically in development of the craniofacial region. Members of this family are vital to development of the secondary palate where they regulate maxillary and palate mesenchymal cell proliferation and extracellular matrix synthesis. The function of this growth factor family is particularly critical in that perturbation of either process results in a cleft of the palate. While the cellular and phenotypic effects of TGFß on embryonic craniofacial tissue have been extensively cataloged, the specific genes that function as downstream mediators of TGFß in maxillary/palatal development are poorly defined. Gene expression arrays offer the ability to conduct a rapid, simultaneous assessment of hundreds to thousands of differentially expressed genes in a single study. Inasmuch as the downstream sequelae of TGFß action are only partially defined, a complementary DNA (cDNA) expression array technology (Clontech's AtlasTM Mouse cDNA Expression Arrays), was utilized to delineate a profile of differentially expressed genes from TGFß-treated primary cultures of murine embryonic maxillary mesenchymal cells. Hybridization of a membrane-based cDNA array (1178 genes) was performed with 32P-labeled cDNA probes synthesized from RNA isolated from either TGFß-treated or vehicle-treated embryonic maxillary mesenchymal cells. Resultant phosphorimages were subject to AtlasImageTM analysis in order to determine differences in gene expression between control and TGFß-treated maxillary mesenchymal cells. Of the 1178 arrayed genes, 552 (47%) demonstrated detectable levels of expression. Steady state levels of 22 genes were up-regulated, while those of 8 other genes were down-regulated, by a factor of twofold or greater in response to TGFß. Affected genes could be grouped into three general functional categories: transcription factors and general DNA-binding proteins; growth factors/signaling molecules; and extracellular matrix and related proteins. The extent of hybridization of each gene was evaluated by comparison with the abundant, constitutively expressed mRNAs: ubiquitin, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), ornithine decarboxylase (ODC), cytoplasmic beta-actin and 40S ribosomal protein. No detectable changes were observed in the expression levels of these genes in response to TGFß treatment. Gene expression profiling results were verified by Real-Time quantitative polymerase chain reaction. Utilization of cDNA microarray technology has enabled us to delineate a preliminary transcriptional map of TGFß responsiveness in embryonic maxillary mesenchymal cells. The profile of differentially expressed genes offers revealing insights into potential molecular regulatory mechanisms employed by TGFß in orchestrating craniofacial ontogeny. [source] | |||||||||||||