Oreda Boussadia

Publications (4)17.33 Total impact

• Article: Conditional inactivation of the E-cadherin gene in thyroid follicular cells affects gland development but does not impair junction formation.

  Gaetano Calì, Mariastella Zannini, Patrizia Rubini, Carlo Tacchetti, Barbara D'Andrea, Andrea Affuso, Tim Wintermantel, Oreda Boussadia, Daniela Terracciano, Daniel Silberschmidt, Elena Amendola, Mario De Felice, Günther Schütz, Rolf Kemler, Roberto Di Lauro, Lucio Nitsch
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  ABSTRACT: We have conditionally inactivated the E-cadherin gene in the thyroid follicular cells of mouse embryo to unravel its role in thyroid development. We used the Cre-loxP system in which the Cre-recombinase was expressed under the control of the tissue-specific thyroglobulin promoter that becomes active at embryonic d 15. At postnatal d 7, thyroid follicle lumens in the knockout mice were about 30% smaller with respect to control mice and had an irregular shape. E-cadherin was almost completely absent in thyrocytes, beta-catenin was significantly reduced, whereas no change in gamma-catenin was detected. alpha-Catenin was also reduced on the cell plasma membrane. Despite the dramatic loss of E-cadherin and beta-catenin, cell-cell junctions were not affected, the distribution of tight junction proteins was unaltered, and no increase of thyroglobulin circulating in the blood was observed. In addition, we found that other members of the cadherin family, the R-cadherin and the Ksp-cadherin, were expressed in thyrocytes and that their membrane distribution was not altered in the E-cadherin conditional knockout mouse. Our results indicate that E-cadherin has a role in the development of the thyroid gland and in the expression of beta-catenin, but it is not essential for the maintenance of follicular cell adhesion.
  Endocrinology 07/2007; 148(6):2737-46. · 4.46 Impact Factor
• Article: E-cadherin controls adherens junctions in the epidermis and the renewal of hair follicles.

  Peter Young, Oreda Boussadia, Hartmut Halfter, Richard Grose, Philipp Berger, Dino P Leone, Horst Robenek, Patrick Charnay, Rolf Kemler, Ueli Suter
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  ABSTRACT: E-cadherin is thought to mediate intercellular adhesion in the mammalian epidermis and in hair follicles as the adhesive component of adherens junctions. We have tested this role of E-cadherin directly by conditional gene ablation in the mouse. We show that postnatal loss of E-cadherin in keratinocytes leads to a loss of adherens junctions and altered epidermal differentiation without accompanying signs of inflammation. Overall tissue integrity and desmosomal structures were maintained, but skin hair follicles were progressively lost. Tumors were not observed and beta-catenin levels were not strongly altered in the mutant skin. We conclude that E-cadherin is required for maintaining the adhesive properties of adherens junctions in keratinocytes and proper skin differentiation. Furthermore, continuous hair follicle cycling is dependent on E-cadherin.
  The EMBO Journal 12/2003; 22(21):5723-33. · 9.20 Impact Factor
• Article: E-cadherin is required for the correct formation of autotypic adherens junctions of the outer mesaxon but not for the integrity of myelinated fibers of peripheral nerves.

  Peter Young, Oreda Boussadia, Philipp Berger, Dino P Leone, Patrick Charnay, Rolf Kemler, Ueli Suter
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  ABSTRACT: The calcium-dependent adhesion protein E-cadherin is present in noncompacted regions of myelin sheaths in the peripheral nervous system. There, it is localized to electron-dense structures between membranes of the same Schwann cell referred to as autotypic adherens junctions. It has been suggested that the failure of E-cadherin-mediated adhesion might cause demyelination that proceeds in certain pathological states. To test the requirement of E-cadherin in peripheral nerves, we used tissue-specific gene ablation techniques based on the Cre/LoxP system. We show that E-cadherin deficiency does not cause significant demyelination up to the age of 15 months. Immunostainings for nodal sodium channels, the paranodal protein Caspr1, and the juxtaparanodal potassium channels Kv1.1 and Kv1.2 revealed that E-cadherin is not necessary to maintain the general functional architecture of the nodal region. On the ultrastructural level, we detected a widening of the outer mesaxon accompanied by a loss of electron-dense cytoplasmic areas. We conclude that E-cadherin is required for the proper establishment and/or the maintenance of the outer mesaxon in myelinated PNS fibers but is dispensable for proper nerve function.
  Molecular and Cellular Neuroscience 11/2002; 21(2):341-51. · 3.66 Impact Factor
• Article: Short title: E-cadherin inactivation in the thyroid gland

  Gaetano Calì, Mariastella Zannini, Patrizia Rubini, Carlo Tacchetti, Barbara D'Andrea, Andrea Affuso, Tim Wintermantel, Oreda Boussadia, Daniela Terracciano, Daniel Silberschmidt, Elena Amendola, Mario De Felice