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Liver fibrosis, the accumulation of extracellular matrix proteins caused by chronic liver damage, results from the activation of hepatic stellate cells. In a new study, Arriazu et al. explore in detail the mechanisms by which the multifunctional protein osteopontin drives hepatic fibrosis, and show that interaction with HMGB1 mediates the fibrogenic response. 
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In this paper, the authors investigate the role of FGF9 thanks to a shRNA LV FGF9. They observe that if the level of expression of FGF9 decreases, the anxiety-like behavior is improved. The authors propose that the relative levels of FGF9 in relation to other members of the FGF family may prove key to understanding vulnerability or resilience in affective disorders.
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In this study, the authors investigate the effect of growth-associated protein-43 (GAP-43) on bone marrow mesenchymal stem cell (BMSC) differentiation in a rat model of traumatic optic neuropathy (TON). They realize GAP‑43 overexpression and GAP‑43 knockdown thanks different lentiviral vectors. In this way, they show that GAP‑43 promoted BMSC differentiation into neuron-like cells, and intravitreally injected GAP-43/BMSCs promoted the process of nerve repair in a rat model of TON.
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employed a conditional RNA interference knockdown strategy with a lentiviral vector encoding a short hairpin p53
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Thanks to a conditional RNA interference knockdown strategy with a lentiviral vector encoding a short hairpin p53, the authors show that skeletal muscle dedifferentiation during newt limb regeneration depends on a programmed cell death response by myofibres.
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In this study, the authors design a lentiviral vectors (LV) for delivery of snoMEN RNAs which is an antisense technology for targeted knock-down of protein coding mRNAs. They show that the vectorization in LV increases the efficiency of delivery in many human cell lines that are difficult to transfect with plasmid vectors. Transduction of lentiviral vectors expressing snoMEN targeted to pri-miR21 induces apoptosis in human lung adenocarcinoma cells, which express high levels of miR21, but not in human primary cells. They show that snoMEN-mediated suppression of miRNA expression is prevented by siRNA knock-down of Ago2, but not by knock-down of Ago1 or Upf1. snoMEN RNAs colocalise with Ago2 in cell nuclei and nucleoli and can be co-immunoprecipitated from nuclear extracts by antibodies specific for Ago2.
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The scientists investigated the effects of HSP27 expression on cytoskeleton dynamics and contractile function of human bladder smooth muscle cells (BSMCs) in vitro. In this goal, they used lentiviral vectors to overexpress or knock down HSP27. They show that the structure of actin filaments in HSP27 over-expressed cells recovered and F/G-actin ratio significantly increased at 12 h after stretching which is not the case in HSP27 knock-down cells. In addition, the contractile force of BSMCs was enhanced by over-expression of HSP27 and attenuated by knock-down of HSP27, suggesting a pivotal role of HSP27 in regulating bladder smooth muscle contraction.
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In this study, the authors used an shRNAlentiviral vector to knockdown the LAPTM4B to study its implication in the human serous adenocarcinoma cell line. They observed that transduced cells exhibited significant decreases in cell motility and invasion. Furthermore, LAPTM4B depletion resulted in a significant decrease in PCNA, VEGF, MMP2, MMP9 and CDK12 expression. These results suggest that LAPTM4B expression may be an oncogene-inducing feature of invasive ovarian cancer cells and may be a potential therapeutic target for ovarian cancer treatment.
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In this study, the authors knock down with a shRNA lentiviral vector the methyl CpG binding protein 2 (MeCP2) which enhances NF-κB activation in human peripheral blood mononuclear cells. They observed that MeCP2 deficiency increases expression of TNFα and other inflammatory cytokines by enhancing NF-κB signaling.
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The authors identified RAGE as the key mediator of HMGB1 effects on HSCs by using lentiviral expression vectors to achieve small hairpin expression knockdown of either TLR2, TLR4 and TLR9 or RAGE, and then showed that only knockdown of RAGE decreased HMGB1-induced collagen expression.