Cell-cell contact preserves cell viability via plakoglobin.
Ontology highlight
ABSTRACT:
SUBMITTER: Wei Q
PROVIDER: S-EPMC3203941 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The main objectives of this work were to assess the efficiency, ease-of-use, and general performance of a novel osseoshaping tool based on first-user clinical experiences and to compare these observations with preclinical data generated in rodents using a miniaturized version of the instrument. All patients selected for the surgery presented challenging clinical conditions in terms of the quality and/or quantity of the available bone. The presented data were collected during the implant placement of 15 implants in 7 patients, and included implant recipient site (bone quality and quantity) and ridge evaluation, intra-operative handling of the novel instrument, and the evaluation of subsequent implant insertion. The instrument was easy to handle and was applied without any complications during the surgical procedure. Its use obviated the need for multiple drills and enabled adequate insertion torque in all cases. This biologically driven innovation in implant site preparation shows improvements in preserving vital anatomical and cellular structures as well as simplifying the surgical protocol with excellent ease-of-use and handling properties.
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Project description:BackgroundEpithelial cell adhesion molecule EpCAM is a transmembrane glycoprotein, which is frequently over-expressed in simple epithelia, progenitors, embryonic and tissue stem cells, carcinoma and cancer-initiating cells. Besides functioning as a homophilic adhesion protein, EpCAM is an oncogenic receptor that requires regulated intramembrane proteolysis for activation of its signal transduction capacity. Upon cleavage, the extracellular domain EpEX is released as a soluble ligand while the intracellular domain EpICD translocates into the cytoplasm and eventually into the nucleus in combination with four-and-a-half LIM domains protein 2 (FHL2) and beta-catenin, and drives cell proliferation.MethodsEpCAM cleavage, induction of the target genes, and transmission of proliferation signals were investigated under varying density conditions using confocal laser scanning microscopy, immunoblotting, cell counting, and conditional cell systems.ResultsEpCAM cleavage, induction of the target genes, and transmission of proliferation signals were dependent on adequate cell-to-cell contact. If cell-to-cell contact was prohibited EpCAM did not provide growth advantages. If cells were allowed to undergo contact to each other, EpCAM transmitted proliferation signals based on signal transduction-related cleavage processes. Accordingly, the pre-cleaved version EpICD was not dependent on cell-to-cell contact in order to induce c-myc and cell proliferation, but necessitated nuclear translocation. For the case of contact-inhibited cells, although cleavage of EpCAM occurred, nuclear translocation of EpICD was reduced, as were EpCAM effects.ConclusionActivation of EpCAM's cleavage and oncogenic capacity is dependent on cellular interaction (juxtacrine) to provide for initial signals of regulated intramembrane proteolysis, which then support signalling via soluble EpEX (paracrine).
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