Current Issue : April - June Volume : 2016 Issue Number : 2 Articles : 5 Articles
Biomedical materials for bone therapy are usually assessed for their biocompatibility and safety employing animal models or in vitro\nmonolayer cell culture assays.However, alternative in vitro models may offer controlled conditions closer to physiological responses\nand reduce animal testing. In this work, we developed a 3D spheroidal cell culture with potential to evaluate simultaneously\nmaterial-cell and cell-cell interactions. Different cell densities of murine MC3T3-E1 preosteoblasts or human primary osteoblasts\n(HOb) were used to determine the ideal procedure of spheroidal cultures and their adequacy to material testing. Cells were seeded\non 96-well plates coated with agar and incubated in agitation from 1 to 7 days. Aggregate morphology was qualitatively evaluated\nconsidering the shape, size, repeatability, handling, and stability of spheroids. Higher cell densities induced more stable spheroids,\nand handling was considered appropriate starting from 2 Ã?â?? 104 cells. Confocal microscopy and Scanning Electron Microscopy\nindicate that most cells within the aggregate core are viable. Exposure to positive controls has shown a dose dependent cell\ndeath as measured by XTT assay. Aggregates were stable and presented good viability when employed on standardized testing\nof metallic and polymer-based biomaterials. Therefore, osteoblast spheroids may provide a promising tool for material screening\nand biocompatibility testing....
Introduction: Stem cells have great therapeutic potential due to their capacity for self-renewal and their potential\nfor differentiating into multiple cell lineages. It has been recently shown that the host immune system has\nfundamental effects on the fate of transplanted mesenchymal stem cells during bone repair, where the topical\nadministration of aspirin is capable of improving calvarial bone repair in rodents by inhibiting tumor necrosis factor-Ã?±\n(TNF-Ã?±) and interferon-Ã?³ (IFN-Ã?³) production. This study investigates whether aspirin is capable of accelerating the\nregenerative potential of bone marrow mesenchymal stem cells (BMSC) in a mini swine calvarial bone defect model.\nMethods: Calvarial bone defects (3 cm Ã?â?? 1.8 cm oval defect) in mini swine were treated with BMSC pretreated\nwith 75 Ã?¼g/ml aspirin for 24 h seeded onto hydroxyaptite/tricalcium phosphatel (HA/TCP), or with BMSC with\nHA/TCP, or with HA/TCP only, or remained untreated. Animals were scanned with micro-computed tomography\n(microCT) at 2 days and 6 months postsurgery and were sacrificed at 6 months postsurgery with decalcified\ntissues being processed for histomorphometric examination. The cytokine levels, including TNF-Ã?± and IFN-Ã?³, were\nmeasured by enzyme-linked immunosorbent assay (ELISA).\nResults: Aspirin at 75 Ã?¼g/ml promoted the osteogenesis of BMSC in vitro and in vivo, shown by Alizarin Red staining\nand new bone volume in the nude mice transplantation model (p < 0.01), respectively. Defects treated with\naspirin-BMSC showed significantly greater new bone fill compared with other three groups at 6 months post surgery\n(p < 0.01). Aspirin-BMSC treatment has significantly decreased the concentration of TNF-Ã?± and IFN-Ã?³ (p < 0.05).\nConclusions: The present study shows that BMSC pretreated with aspirin have a greater capacity to repair calvarial\nbone defects in a mini swine model. The results suggest that the administration of aspirin is capable of improving\nBMSC-mediated calvarial bone regeneration in a big animal model....
Fibrosis of organs is observed in systemic autoimmune disease. Using a scleroderma\nmouse, we show that transplantation of MHC compatible, minor antigen mismatched bone marrow\nstromal/stem cells (BMSCs) play a role in the pathogenesis of fibrosis. Removal of donor BMSCs\nrescued mice from disease. Freshly isolated PDGFRa\n+ Sca-1+ BMSCs expressed MHC class II\nfollowing transplantation and activated host T cells. A decrease in FOXP3+ CD25+ Treg population\nwas observed. T cells proliferated and secreted IL-6 when stimulated with mismatched BMSCs in\nvitro. Donor T cells were not involved in fibrosis because transplanting T cell-deficient RAG2 knock\nout mice bone marrow still caused disease. Once initially triggered by mismatched BMSCs, the\nautoimmune phenotype was not donor BMSC dependent as the phenotype was observed after\neffector T cells were adoptively transferred into na�±�¨ve syngeneic mice. Our data suggest that minor\nantigen mismatched BMSCs trigger systemic fibrosis in this autoimmune scleroderma model.\nDOI: 10.7554/eLife.09394.001...
Background: Ovarian cancer is a possibly lethal gynecological malignancy and this study utilized phage display\ntechnology to screen and identify peptides that specifically bind to ovarian cancer cells and explored the effects of\nthese peptides on ovarian cancer cells in vitro and in vivo.\nMethods: The phage displayed peptide library was used to isolate the peptides binding to and internalizing into\nthe ovarian carcinoma cells. Positive phage clones were characterized with DNA sequencing and bioinformatics\nanalysis and then validated with immunofluorescence. Subsequently, the selected peptides were investigated for\ntheir cancer-related functions, including cell adhesion, spreading, motility, and invasion in vitro and in vivo.\nResults: Peptide1 read as SWQIGGNwas the positive peptide and showed preferential binding to the target cells.\nPeptide 1 also inhibited cell proliferation, migration, invasion and adhesion of ovarian cancer HO8910 cells in vitro.\nIn vivo, Peptide 1 led to a lower tumorigenicity of HO8910 cells, which was characterized by the inhibitory effect on\ntumor growth and metastasis of ovarian cells.\nConclusion: These studies demonstrate that the phage display-identified tumor cell-binding peptide was able to\ncontrol ovarian cancer cell viability, migration, invasion, and adhesion capacity in vitro as well as tumor growth and\nmetastasis in vivo. Future studies will be aimed at evaluating the clinical efficacy of the peptide SWQIGGN in ovarian\ncancer patients....
Background: Morphine is used widely to treat severe pain in some medical conditions including cancer. Previous studies have shown conflicting reports about the effect of this analgesic drug on the proliferation and growth of various cancer cells. The aim of the present study was determining the effect of this drug (20-600 ) on the proliferation of ovarian cancer A2780cp cell line. To investigate the effect of morphine on A2780cp cell line, morphological changes were studied with inverted microscope, the viability of cells was determined with trypan blue staining and MTT assay, and the type of cell death was determined using flow cytometry analysis. Results: Morphological and molecular analysis have revealed traces of apoptosis. Trypan blue staining and MTT assay have shown deceasing of viability in does and time dependent manners with IC50 from 385-510 for 24-72 hours. Flowcytometry analyzes revealed 20.97% apoptosis after treatment with 300 morphine for 48 hours. Discussion: Our findings suggest that morphine can reduce the proliferation and growth of A2780cp cell line with inducing apoptosis more than necrosis in this type of cells....
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