Roles of magnesium and calcium ions in cell-to-substrate adhesion.
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Biomedical subjects
Publications and source records attributed to M Takeichi.
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Selective adhesive properties of cells are thought to have a key role in animal morphogenesis, but the molecular bases underlying these properties remain to be determined. Our studies have demonstrated that cell-type-specific adhesiveness resides in a class of cell-cell adhesion molecules, termed cadherins, which were defined as the molecular components of the Ca2+-dependent cell adhesion system (CADS). For example, a cadherin molecule identified in mouse teratocarcinoma cells, termed E-cadherin (this molecule seems to be identical to uvomorulin or cell-CAM 120/80 and equivalent to chicken L-CAM), was detected only in epithelial cells of various organs; it did not cross-react with cadherins on other cell types. We recently described a novel type of cadherin, N-cadherin, which is found in mouse cells and whose tissue distribution is distinct from that of E-cadherin. In the present study, we have identified a molecular component of N-cadherin in the chicken and determined its distribution in the tissues of early embryos. The results suggest that expression of this adhesion molecule is associated with separation and sealing of cell layers in morphogenesis.
E-cadherin is a cell surface glycoprotein responsible for Ca2+-dependent intercellular adhesion between epithelial cells; it is also called uvomorulin, L-CAM (ref. 3), cell-CAM 120/80 (ref.4) or Arc-1 (ref. 5). Because blocking the action of E-cadherin by monoclonal antibodies causes dispersion of compact cell colonies, this molecule is thought to be an important factor for maintenance of multicellular systems. To demonstrate directly that E-cadherin is involved in cell-cell adhesion, we cloned full-length cDNA encoding E-cadherin from F9 cells and introduced it into L fibroblasts deficient in E-cadherin. These L cells acquire strong Ca2+-dependent aggregating activity by expressing the E-cadherin derived from the introduced cDNA and were morphologically transformed so as to form colonies in which cells were tightly connected to each other.
In order to elucidate the antitumor effect and mechanism of action of photodynamic therapy (PDT) using the photosensitizing agent mono-L-aspartyl chlorin e6 (NPe6) and a semiconductor laser, we conducted a morphologic study on uterine cervical cancer cell lines. First, tumor shrinkage was confirmed in a tumor growth inhibition test. Next, morphologic changes after PDT were examined, and since the major change appeared to be tumor necrosis secondary to obstruction of the blood vessels around the tumor, an NPe6 cell uptake experiment was performed. The results confirmed that a significantly greater amount of NPe6 was incorporated by human umbilical vein endothelial cells (HUV-EC1) and the cervical cancer cell lines than by human umbilical cord-derived fibroblasts. Based on these findings it was concluded that NPe6 possesses tumor affinity, and necrosis secondary to vascular obstruction was postulated to be the principal mechanism of the antitumor effect of PDT using NPe6.
The CT appearance of bronchiectasis on inspiration and expiration in a patient with congenital bronchiectasis due to cartilage deficiency (Williams-Campbell syndrome) is reported. Computed tomography demonstrated characteristic findings of this syndrome, ballooning of bronchi on inspiration and collapse on expiration.