ABSTRACT
The transcription factor grainy head (Grh) functions in the protection of the epithelium against the external environment by generating strongly adhesive layers, and this function is conserved in vertebrates and invertebrates. In Drosophila, the top model for holometabolous insects, Grh is necessary during embryonic development, epidermal differentiation, central nervous system specification and epithelial repair. However, the function of this gene in hemimetabolous insect epithelia remains unknown. To examine the function of Grh signaling in regulating epithelium development in Hemimetabola, we focused on the Blattella germanica epidermal layer using a gene knockdown strategy. The spatiotemporal expression pattern of BgGrh was detected, and knockdown of BgGrh and BgCad96ca, which provide positive feedback to BgGrh, caused severe defects in new epithelium development and impeded the molting process required to discard the old integument. Knockdown of the expression of BgGrh and BgCad96ca caused increased expression of chitin synthase gene (BgCHS1) and chitinase gene (BgCht5), the upregulations of which should be mediated by the higher level of hormone receptor 3 (BgHr3) gene. In conclusion, epithelium development is regulated by Grh signaling, which might represent a potential target for the control of urban pest cockroaches.
Subject(s)
Blattellidae/growth & development , Epithelium/growth & development , Insect Proteins/genetics , Molting/genetics , Animals , Blattellidae/genetics , Insect Proteins/metabolism , Nymph/genetics , Nymph/growth & developmentABSTRACT
El uso del hidróxido de calcio desde hace más de 90años en el campo de la endodoncia, ha establecido su seguridad limitando sus efectos adversos a efectos localizados. Sin embargo, su elevado pHy un cierto grado de citotoxicidad lo hacen un material no biocompatible per se. Los efectos adversos notificados derivados de la extrusión de hidróxido de calcio al periápice, aunque escasos, son muy variados: granulomas y quistes, antrolitos dentro del seno maxilar, necrosis de la mucosa por contacto directo, parestesia óhipoestesia del nervio dentario inferior, incluso severas necrosis faciales. Los factores que influyen en la extrusión y que contribuyen de forma negativa en la formación de las lesiones son la densidad de la preparación de Ca (OH)2, sus métodos de inserción, factores anatómicos determinantes, las situaciones iatrogénicas a tener en cuenta y la intencionalidad del operador debida a su indicación. En este trabajo se establecen recomendaciones para la prevención y el tratamiento precoz de estos problemas en pos de la seguridad del paciente odontológico (AU)
The use of calcium hydroxide for more than 90years in the field of endodontics has established its safety limiting its adverse effects to localized effects. However, its high pH and a certain degree of cytotoxicity make it a non-biocompatible material per se. The reported adverse effects derived from the extrusion of calcium hydroxide to the periapex, though few, are quite varied: granulomas and (..) (AU)
Subject(s)
Humans , Orthodontic Extrusion/adverse effects , Calcium Hydroxide/adverse effects , Periapical Tissue , /epidemiologyABSTRACT
Endothelial barrier dysfunction leading to increased permeability and vascular leakage is an underlying cause of several pathological conditions. Whereas these changes have been shown to be associated with activation of the complement system, leading to the release of C5a and interaction of C5a-C5a receptor (C5aR), the role of C5aR in endothelial cells remain(s) ill-defined. Here, we report an essential role of C5aR in endothelial cell injury and vascular permeability through silencing of the C5aR gene using siRNA. In the cultured mouse dermal microvascular endothelial cells (MEMECs) monolayer transfected with C5aR-siRNA, endotoxin-induced cell injury by evaluated as transendothelial flux, cell detachment, and cytoskeletal disorganization was inhibited. Upregulation of vascular cell adhesion molecule-1 (VCAM-1) was also suppressed. Studies exploring the underlying mechanism of siRNA-mediated suppression in VCAM-1 expression were related to reduction of NF-kappaB activation and nuclear localization of both p50 and p65. The effect was associated with inhibition in activation of protein kinase Cdelta(PKC-delta) and induction of PKC-mediated mitogen-activated protein kinase phosphatases-1 (MKP-1) leading to the increased activity of p42/p44 mitogen-activated protein (MAP) kinase cascade. In the model of mice administrated with C5aR-siRNA, endotoxin-induced plasma leakage was inhibited in local abdominal skin. Systemic administration of endotoxin to mice resulted in increased microvascular permeability in multiple organs was reduced. These studies demonstrate that the C5aR responsible for vascular endothelial cell injury and plasma permeability is an important factor, and that blockade of C5aR may be useful therapeutic targets for the prevention of vascular permeability in pathogenic condition.
