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MEE Cells (mee + cell)

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Life Sciences	100%

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Morphological and immunohistochemical studies on cleft palates induced by 2,3,7,8-tetrachlorodibenzo- p -dioxin in mice

CONGENITAL ANOMALIES, Issue 2 2008
Kumiko Fujiwara
ABSTRACT Morphological and immunohistological examinations were performed to reveal the mechanisms of cleft palate induction by 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD). ICR strain mice 8,10 weeks of age were used in the study. TCDD was administered in olive oil on gestation day (GD) 12.5 with gastric tubes at 40 ,g/kg. From GD 13.5 to 16.5, palates were examined by scanning electron microscopy (SEM), hematoxyline,eosin (HE) staining, and immunohistochemical staining of FGFR1/2, TGF-,3, MSX1 and LHX8. In the control group, both of the palatal shelves began elevating on GD 14.0 and finished within 6 h. After the elevation, all of the shelves had completely fused with each other on GD 14.5. In the TCDD-treated group, palatal shelves elevated 1 day later than in the control group. However, all palates had elevated by GD 15.0. After the elevation, the shelves contacted each other and fused; however, they were separated on GD16.0. HE staining showed that medial edge epithelium (MEE) was thinner in the TCDD group than in the control group. MEE observed under a high magnification (×2500) exhibited filopodia-like filaments and the cells were bulged in the control group. In contrast, in the TCDD group, no filaments were observed and the cells were flat with unclear boundaries. Immunohistologically, there were no characteristic findings except for FGFR1. FGFR1 was not expressed in the TCDD group after the fusion phase (GD 14.5). TCDD induces many morphological and molecular changes to MEE cells and causes cleft palates. [source]

The role of twist during palate development,

DEVELOPMENTAL DYNAMICS, Issue 10 2008
Wenli Yu
Abstract In palatogenesis, the MEE (Medial Edge Epithelium) cells disappear when palates fuse. We hypothesize that the MEE cells undergo EMT (Epithelial-Mesenchymal Transition) to achieve mesenchyme confluence. Twist has an important role in EMT for tumor metastasis. The purpose of this study was to analyze Twist function during palatal fusion. Twist protein was expressed in palatal shelves and MEE both in vivo and in vitro just prior to fusion. Twist mRNA increased in chicken palates 3 and 6 hr after TGF,3 treatment. Palatal fusion was decreased when cultured palatal shelves were treated with 200 nM Twist siRNA and the subcellular localization of ,-catenin was altered. Twist mRNA decreased in palatal shelves treated with TGF,3 neutralizing antibody or LY294002, a specific phosphatidylinositol-3 kinase (PI-3K) inhibitor. In summary, Twist is downstream of TGF,3 and PI-3K pathways during palatal fusion. However, decreasing Twist with siRNA did not completely block palate fusion, indicating that the function of Twist may be duplicated by other transcription factors. Developmental Dynamics 237:2716,2725, 2008. © 2008 Wiley-Liss, Inc. [source]

Inhibition of SMAD2 expression prevents murine palatal fusion

DEVELOPMENTAL DYNAMICS, Issue 7 2006
Nobuyuki Shiomi
Abstract Transforming growth factor (TGF)-beta 3 is known to regulate the disappearance of murine medial edge epithelium (MEE) during palatal fusion. Our previous studies showed that SMAD2, a TGF-beta signaling mediator, was expressed and phosphorylated primarily in the MEE and that SMAD2 phosphorylation in the MEE was temporospatially regulated by TGF-beta 3. The goal of this study was to examine the requirement for SMAD2 to complete the developmental events necessary for palatal fusion. SMAD2 expression was inhibited with Smad2 siRNA transfection into palatal tissues in vitro. The results showed that Smad2 siRNA transfection resulted in the maintenance of MEE cells in the palatal midline. Western blot and immunofluorescence analyses confirmed that the endogenous SMAD2 and phospho-SMAD2 levels were reduced following siRNA transfection. The SMAD3 level was not altered by the Smad2 siRNA transfection. The persistence of the MEE and the decreased SMAD2/phospho-SMAD2 levels were coincident with increased MEE cell proliferation. Addition of exogenous TGF-beta 3 increased p-SMAD2 level but not the total SMAD2 level. Therefore, exogenous TGF-beta 3 was not able to induce p-SMAD2 enough to rescue the palatal phenotype in the Smad2 siRNA group. The results indicated that the endogenous SMAD2 level is crucial in the regulation of disappearance of MEE during palatal fusion. Developmental Dynamics 235:1785,1793, 2006. © 2006 Wiley-Liss, Inc. [source]

TGF-,3,dependent SMAD2 phosphorylation and inhibition of MEE proliferation during palatal fusion

DEVELOPMENTAL DYNAMICS, Issue 3 2003
Xiao-Mei Cui
Abstract Transforming growth factor (TGF) -,3 is known to selectively regulate the disappearance of murine medial edge epithelium (MEE) during palatal fusion. Previous studies suggested that the selective function of TGF-,3 in MEE was conducted by TGF-, receptors. Further studies were needed to demonstrate that the TGF-, signaling mediators were indeed expressed and phosphorylated in the MEE cells. SMAD2 and SMAD3 were both present in the MEE, whereas SMAD2 was the only one phosphorylated during palatal fusion. SMAD2 phosphorylation was temporospatially restricted to the MEE and correlated with the disappearance of the MEE. No phosphorylated SMAD2 was found in MEE in TGF-,3,/, mice, although nonphosphorylated SMAD2 was present. The results suggest that TGF-,3 is required for initiating and maintaining SMAD2 phosphorylation in MEE. Phospho-SMAD3 was not detectable in palate during normal palatal fusion. Previous results suggested TGF-,,induced cessation of DNA synthesis in MEE cells during palatal fusion in vitro. The present results provide evidence that inhibition of MEE proliferation in vivo was controlled by endogenous TGF-,3. The number of 5-bromo-2,-deoxyuridine (BrdU) -labeled MEE cells was significantly reduced in TGF-,3+/+ compared with TGF-,3,/, mice when the MEE seam formed (t -test, P < 0.05). This finding suggests that TGF-,3 is required for inhibiting MEE proliferation during palatal fusion. The inhibition of MEE proliferation may be mediated by TGF-,3,dependent phosphorylation of SMAD2. Developmental Dynamics 227:387,394, 2003. © 2003 Wiley-Liss, Inc. [source]