Browsing by Subject "Tight junction"

Now showing 1 - 5 of 5
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    Analysis of cell-cell junctions in human amnion and chorionic plate affected by chorioamnionitis
    (2016) Licini, Caterina; Tossetta, Giovanni; Avellini, Chiara; Ciarmela, Pasquapina; Lorenzi, Teresa; Toti, Paolo; Gesuita, Rosaria; Voltolini, Chiara; Petraglia, Felice; Castellucci, Mario; Marzioni, Daniela
    Chorioamnionitis is an acute inflammatory reaction associated with the premature rupture of the fetal membranes. It is caused mainly by invasion of bacteria from the vaginal tract that can penetrate the intact membranes and invade the amnion cavity and the decidua. Tight junctions (TJ) and adherent junctions (AJ) are intercellular junctions crucial for epithelia adhesion and permeability regulation in a wide variety of tissues and organs. Our aim is to investigate if TJ and AJ molecules are involved in human chorioamnionitis. We studied the protein expression (by immunohistochemistry and western blotting) and the mRNA levels (by RT-PCR) of some junction proteins such as Zonula Occludens-1 (ZO-1), occludin, VE-cadherin and βcatenin in fetal membranes from women with chorioamnionitis compared to those membranes derived from idiopathic pregnancies. Western blotting and immunohistochemical data established that occludin expression was decreased in amnion with chorioamnionitis compared to amnion from idiopathic pregnancies. Samples tested for ZO-1, VEcadherin and β-catenin (proteins and mRNAs) showed no differences between idiopathic and pathological membranes. One of the most relevant results is the decrease of occludin in membranes with chorioamnionitis. Since we have previously demonstrated that some cytokines, particularly elevated in the chorioamnionitis, cause the disruption of TJs in placental villi, we suggest that the decrease of occludin in amnion may be the first change that leads to the rupture of the amniotic membrane in this pathology.
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    Claudin-1 role in colon cancer: An update and a review
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Ouban, Abderrahman
    Tight junction proteins are essential for sealing the cellular sheets and controlling para-cellular ion flux. Our understanding of the role that tight junction proteins, particularly claudins, play in cellular functions and pathologic conditions is continuously expanding. Particularly, the role of claudin-1 in oncogenesis in multiple locations in the human body is coming to light. This review will shed light on the role of claudin-1 in colon cancer. It will address the mechanisms through which claudin-1 becomes dysregulated in colon cancer. This will provide a platform to address results of claudin-1 expression in the third most common malignant tumour worldwide. Furthermore, it will provide updates about possible use of this biomarker in the surveillance of difficult colon maladies, such as inflammatory bowel disease. The use of claudin-1 as a biomarker of diagnostic and prognostic values will provide Medicine with much needed ammunition in the fight against cancer and will bring about, with added refinements, a new chapter in the era of personalized medicine to tackle this disease and match its destructive course with equally powerful and specifically targeted therapies.
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    Dynamic assembly of tight junction-associated proteins ZO-1, ZO-2, ZO-3 and occludin during mouse tooth development
    (Murcia : F. Hernández, 2003) Unda, F.; Pérez-Nanclares, G.; Le Morvan, V.; Hernández, C.; Vilaxa, A.; De-la-Fuente, M.; Gorry, P.
    Tight junctions might play a role during tissue morphogenesis and cell differentiation. In order to address these questions, we have studied the distribution pattern of the tight junction-associated proteins ZO-1, ZO-2, ZO-3 and occludin in the developing mouse tooth as a model. A specific temporal and spatial distribution of tight junction-associated proteins during tooth development was observed. ZO-1 appeared discontinuously in the cell membrane of enamel organ and dental mesenchyme cells. However, endothelial cells of the dental mesenchyme capillaries displayed a continuous fluorescence at the cell membrane. Inner dental epithelium first showed an evident signal for ZO- 1 at the basal pole of the cells at bud/cap stage, but ZO-1 was accumulated at the basal and apical pole of preameloblast/ameloblasts at late bell stage. Surprisingly, in the incisor ZO-1 decreased as the inner dental epithelium differentiated, and was re-expressed in secretory and mature ameloblasts. On the contrary, ZO-2 was confined to continuous cell-cell contacts of the enamel organ in both molars and incisors. The lateral cell membrane of inner dental epithelial cells was specifically ZO-2 labeled. However, ZO-3 was expressed in oral epithelium whereas dental embryo tissues were negative. In addition, occludin was hardly detected in dental tissues at the early stage of tooth development, but was distributed continuously at the cell membrane of endothelial cells of ED19.5 dental mesenchyme. In incisors, occludin was detected at the cell membrane of the secretory pole of ameloblasts. The occurrence and relation during tooth development of tight junction proteins ZO-1, ZO-2 and occludin, but not ZO-3, suggests a combinatory assembly in tooth morphogenesis and cell differentiation.
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    Emerging relationship between CFTR, actin and tight junction organization in cystic fibrosis airway epithelium
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2017) Castellani, Stefano; Favia, Maria; Guerra, Lorenzo; Carbone, Anna Lucia; Abbattiscianni, Anna Claudia; Di Gioia, Sante; Casavola, Valeria; Conese, Massimo
    Cystic fibrosis (CF), one of the most common genetic disorders affecting primarily Caucasians, is due to mutations in the CF Transmembrane Conductance Regulator (CFTR) gene, encoding for a chloride channel also acting as regulator of other transmembrane proteins. In healthy subjects, CFTR is maintained in its correct apical plasma membrane location via the formation of a multiprotein complex in which scaffold proteins (such as NHERF1) and signaling molecules (such as cAMP and protein kinases) guarantee its correct functioning. In CF, a disorganized and dysfunctional airway epithelium brings an altered flux of ions and water into the lumen of bronchioles, consequent bacterial infections and an enormous influx of inflammatory cells (mainly polymorphonuclear neutrophils) into the airways. Recent evidence in healthy airway cells supports the notion that CFTR protein/function is strictly correlated with the actin cytoskeleton and tight junctions status. In CF cells, the most frequent CFTR gene mutation, F508del, has been shown to be associated with a disorganized actin cytoskeleton and altered tight junction permeability. Thus, the correct localization of CFTR on the apical plasma membrane domain through the formation of the scaffolding and signaling complex is likely fundamental to determine a physiological airway epithelium. The correction of CFTR mutations by either gene or drug therapies, as well as by stem cell-based interventions, can determine the resumption of a physiological organization of actin stress fibers and TJ structure and barrier function, further indicating the close interrelationship among these processes.
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    Renal clear-cell carcinoma: an ultrastructural study on the junctional complexes
    (Murcia : F. Hernández, 2005) Kim, G.; Rajasekaran, Sigrid A.; Thomas, G.; Rosen, E.A.; Landaw, E.M.; Shintaku, P.; Lassman, C.; Said, J.; Rajasekaran, Ayyappan K.
    Junctional complexes such as tight junctions, adherens junctions, and desmosomes play crucial roles in the structure and function of epithelial cells. These junctions are involved in increasing cell-cell contact and as well serve as signaling centers regulating multiple functions in epithelial cells. Carcinoma cell lines cultured in the laboratory generally lack junctional complexes. However, studies directed towards understanding the distribution of junctional complexes in human cancer tissues are lacking. In this study, we analyzed by electron microscopy the distribution of junctional complexes in patients diagnosed with renal clear-cell carcinoma. We found that both tight junctions and adherens junctions were drastically reduced in patients with cancer compared to normal tissues. Desmosomes were not detected in normal proximal tubules while distinctly present in cancer tissues. These results suggest that analysis of junctional complexes in human tumors should provide valuable information that might have prognostic and diagnostic value.