Special Issue "Frontiers of Marine Biomaterials"
Deadline for manuscript submissions: closed (31 July 2016)
The principal motivation for this Special Issue is to use modern knowledge about the nano- and ultrastructural organization, as well as about the physico-chemical and materials properties of biological materials of marine origin. These include a broad variety of mineralized tissues, filaments, fibers, and nanostructured networks found in marine unicellular eukaryotes, such as diatoms, radiolarians, and dinoflagellates, and in multicellular invertebrates, such as sponges, corals, worms, molluscs, echinoderms, and arthropods. Additionally, biocomposites and biopolymers isolated from, and observed in, the diverse range of marine vertebrates (fishes, reptiles, birds, mammals) are of special interest. Once we understand the origin, nature, evolution, and structure–function relationship in materials that are made in marine living systems, we can then use these principles for biomimetic fabrication, design, and self-assembly of new hybride mineralized biopolymer composites for future biomedical and technical applications.
Prof. Dr. Hermann Ehrlich
Manuscript Submission Information
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Authors: Ariane Chan, Ian Paterson, John H. Miller
Abstract: Induction of premature senescence can be an effective anti-tumour action, similar to mitotic block and induction of apoptosis. Little information is available on induction of senescence by microtubule-targeting drugs. In the present study, the induction of senescence in cell cultures by the microtubule-stabilizing agents peloruside A, paclitaxel, and discodermolide, and, as a positive control, the DNA-damaging agent doxorubicin, was investigated using a b-galactosidase (SA-b-gal) assay to assess the presence of a senescence phenotype, a 5-ethynyl-2'-deoxyuridine (EdU)) incorporation assay coupled to flow cytometry to determine if DNA synthesis was inhibited, and a clonogenic assay to assess whether senescent cells were proliferating or not. Since senescence often leads to activation of the p53 and pRb tumour suppressor pathways, Western blotting was also carried out to determine if these two proteins were upregulated during the induction of premature senescence. The concentrations of all four drugs that were able to increased SA-β-gal activity also significantly showed a reduction in clonogenic survival. As expected, doxorubicin was the most effective at inducing a senescent phenotype, followed in order of potency by discodermolide, paclitaxel, then peloruside. A peak in p53 was seen followed by a subsequent decrease back to control levels following treatment with three of the four compounds, including peloruside A and discodermolide, but not paclitaxel. A significant decrease in pRb in response to all four drugs suggested that, like p53 and p21, pRb was not involved in maintaining the senescent phenotype. With regard to the senescent action of peloruside A, it was concluded that at low concentrations, premature senescence played an important, but not predominant, role in its mode of action.