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1.
Viruses ; 15(6)2023 06 17.
Article in English | MEDLINE | ID: mdl-37376685

ABSTRACT

Several oncogenic viruses are associated with approximately 20% of human cancers. Experimental models are crucial for studying the pathogenicity and biological aspects of oncogenic viruses and their potential mechanisms in tumorigenesis. Current cell models have considerable limitations such as: their low yield, genetic and epigenetic modification, and reduction in tumor heterogeneity during long propagation. Cancer cell lines are limited and not appropriate for studying the viral life cycle, for example, natural viral life cycles of HPV and EBV, and their persistence and latency in epithelial cells are poorly understood, since these processes are highly related to epithelial differentiation. Therefore, there is an urgent need of reliable human physiological cell models to study viral life cycle and cancer initiation. Conditional cell reprogramming (CCR) is a rapid and robust cell culture system, where the cells can be established from minimally invasive or noninvasive specimens and their lineage functions preserved during the long-term culture. These CR cells retain their ability to differentiate at air-liquid interface (ALI). Here, we recapitulated the applications of CR and ALI approaches in modeling host-virus interactions and viral-mediated tumorigenesis.


Subject(s)
Carcinoma , Papillomavirus Infections , Humans , Animals , Cellular Reprogramming , Herpesvirus 4, Human/genetics , Oncogenic Viruses , Papillomavirus Infections/pathology , Epithelial Cells , Life Cycle Stages , Carcinogenesis
2.
Oxid Med Cell Longev ; 2013: 186795, 2013.
Article in English | MEDLINE | ID: mdl-23710283

ABSTRACT

Acute bacterial inflammation is accompanied by excessive release of bacterial toxins and production of reactive oxygen and nitrogen species (ROS and RNS), which ultimately results in redox stress. These factors can induce damage to components of tissue barriers, including damage to ubiquitous mesenchymal stromal cells (MSCs), and thus can exacerbate the septic multiple organ dysfunctions. The mechanisms employed by MSCs in order to survive these stress conditions are still poorly understood and require clarification. In this report, we demonstrated that in vitro treatment of MSCs with lipopolysaccharide (LPS) induced inflammatory responses, which included, but not limited to, upregulation of iNOS and release of RNS and ROS. These events triggered in MSCs a cascade of responses driving adaptive remodeling and resistance to a "self-inflicted" oxidative stress. Thus, while MSCs displayed high levels of constitutively present adaptogens, for example, HSP70 and mitochondrial Sirt3, treatment with LPS induced a number of adaptive responses that included induction and nuclear translocation of redox response elements such as NFkB, TRX1, Ref1, Nrf2, FoxO3a, HO1, and activation of autophagy and mitochondrial remodeling. We propose that the above prosurvival pathways activated in MSCs in vitro could be a part of adaptive responses employed by stromal cells under septic conditions.


Subject(s)
Inflammation/pathology , Lipopolysaccharides/pharmacology , Mesenchymal Stem Cells/metabolism , Sepsis/pathology , Animals , Cell Nucleus/drug effects , Cell Nucleus/metabolism , Fluorescent Antibody Technique , Inflammation/metabolism , Mesenchymal Stem Cells/drug effects , Mesenchymal Stem Cells/ultrastructure , Mice , Mitochondria/drug effects , Mitochondria/metabolism , Mitochondria/ultrastructure , NF-kappa B/drug effects , NF-kappa B/metabolism , NF-kappa B/ultrastructure , Nitric Oxide/metabolism , Nitric Oxide Synthase Type II/metabolism , Oxidation-Reduction/drug effects , Phagosomes/drug effects , Phagosomes/metabolism , Phagosomes/ultrastructure , Reactive Nitrogen Species/metabolism , Reactive Oxygen Species/metabolism , Response Elements/genetics , Sepsis/metabolism , Thioredoxins/metabolism , Transcription Factor RelA/metabolism , Transcription, Genetic/drug effects
3.
Cell Biosci ; 3(1): 36, 2013 Sep 16.
Article in English | MEDLINE | ID: mdl-24499553

ABSTRACT

BACKGROUND: Our previous research demonstrated that one subcutaneous injection of 17-Dimethylaminoethylamino-17-demethoxygeldanamycin (17-DMAG) 24 hours (h) before irradiation (8.75 Gy) increased mouse survival by 75%. However, the protective mechanism of 17-DMAG is currently unknown. The present study aimed to investigate whether oral administration of 17-DMAG was also radioprotective and the potential role it may play in radioprotection. RESULTS: A single dose of orally pre-administered (24, 48, or 72 h) 17-DMAG (10 mg/kg) increased irradiated mouse survival, reduced body weight loss, improved water consumption, and decreased facial dropsy, whereas orally post-administered 17-DMAG failed. Additional oral doses of pre-treatment did not improve 30-day survival. The protective effect of multiple pre-administrations (2-3 times) of 17-DMAG at 10 mg/kg was equal to the outcome of a single pre-treatment. In 17-DMAG-pretreated mice, attenuation of bone marrow aplasia in femurs 30 days after irradiation with recovered expressions of cluster of differentiation 34, 44 (CD34, CD44), and survivin in bone marrow cells were observed. 17-DMAG also elevated serum granulocyte-colony stimulating factor (G-CSF), decreased serum fms-related tyrosine kinase 3 ligand, and reduced white blood cell depletion. 17-DMAG ameliorated small intestinal histological damage, promoted recovery of villus heights and intestinal crypts including stem cells, where increased leucine-rich repeat-containing G-protein coupled receptor 5 (Lgr5) was found 30 days after irradiation. CONCLUSIONS: 17-DMAG is a potential radioprotectant for bone marrow and small intestine that results in survival improvement.

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