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We therefore hypothesized that enhancing cell sheet properties by introducing overexpression of a gene associated with angiogenesis, anti-fibrosis, and antiapoptosis could further promote sheet therapy.
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FGFs especially FGF8 promoted sheet-like architecture, cell proliferation, and survival as compared to the control.
Interestingly, the researchers observed that VEGF gradients can lead to different sprout morphology: positive VEGF gradients defined as invasion towards the source of VEGF induced filopodial extensions analogous to tip cell sprouts seen in vivo, but negative gradients instead promoted sheet-like migration analogous to vessel dilation.
When ES-derived cardiomyocytes alone were seeded onto temperature-responsive culture dishes, cell sheets were not created, whereas cocultures with cardiac fibroblasts promoted cell sheet formation.
These experiments suggest that ER reshaping events, specifically those promoting membrane sheet formation from tubules, are crucial for NE assembly.
These results are consistent with the notion that golli promotes process/membrane sheet formation, taking OPCs to an apparently more mature morphological state.
Low 2,2,2,-trifluoroethanol concentration promoted β-sheet structures in SP-BN, which bind Thioflavin T, at acidic pH, whereas it promoted coiled coil structures at neutral pH.
Angiogenic factors such as VEGF-A in the osteogenic matrix cell sheet may promote revascularization and vascular flow.
In fact, those factors produced by L6-HGF sheets were superior to ones produced by L6-WT sheets to promote vWF and SMA-positive cell, but not fibroblast, migration.
We aimed to investigate whether EPCs can enhance the osteogenic properties of MSCs in vitro, and whether transplantation of EPC-MSC cell sheets could promote bone regeneration in a rat model of alveolar bone defect.
Sequences of amino acids with high β-sheet propensities promote assembly into one-dimensional nanostructures in water.
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