Cellular prion protein regulates the differentiation and function of adipocytes through autophagy flux.

The role of autophagy modulation in adipogenic differentiation and the possible autophagy modulators targeting adipogenesis remain unclear. In this study, we investigated whether normal cellular prion protein (PrP) is involved in the modulation of autophagy and affects adipogenic differentiation in vivo and in vitro. Surprisingly, autophagy flux signals were activated in the adipose tissue of prion protein-deficient mice and PrP-deleted 3T3-L1 adipocytes.

Inhibition of Autophagy by Captopril Attenuates Prion Peptide-Mediated Neuronal Apoptosis via AMPK Activation.

Accumulation of prion protein (PrPc) into a protease-resistant form (PrPsc) in the brains of humans and animals affects the central nervous system. PrPsc occurs only in mammals with transmissible prion diseases. Prion protein refers to either the infectious pathogen itself or the main component of the pathogen.

AMPK Activation Mediated by Hinokitiol Inhibits Adipogenic Differentiation of Mesenchymal Stem Cells through Autophagy Flux.

Background And Purpose: Hinokitiol, a natural monopenoid present in the essential oil of heartwood, exerts potent anticancer, anti-inflammatory, antibacterial, and neuroprotective effects on various cells. However, the antiobesity effect of hinokitiol on adipocytes is unclear.

Experimental Approach: In this study, we observed that hinokitiol affected the differentiation to adipocytes in mesenchymal stem cells (MSCs).

Author Correction: Bisphosphonate enhances TRAIL sensitivity to human osteosarcoma cells via death receptor 5 upregulation.

After publication of this article, the authors noticed an error in the figure section.

Resveratrol sensitizes lung cancer cell to TRAIL by p53 independent and suppression of Akt/NF-κB signaling.

Aims: TRAIL is a promising anticancer agent that has the potential to sensitize a wide variety of cancer or transformed cells by inducing apoptosis. However, resistance to TRAIL is a growing concern. Current manuscript aimed to employ combination treatment to investigate resveratrol induced TRAIL sensitization in NSCLC.

Ophiopogonin B sensitizes TRAIL-induced apoptosis through activation of autophagy flux and downregulates cellular FLICE-like inhibitory protein.

Tumor necrosis factor related apoptosis-inducing ligand (TRAIL), a type II transmembrane protein, belongs to the TNF superfamily. Compared to other family members, TRAIL is a promising anti-cancer agent that can selectively induce apoptosis of various types of transformed cells and xenografts, with negligible cytotoxicity against normal tissues. Ophiopogonin B is a bioactive ingredient of Radix , which is frequently used in traditional Chinese medicine to treat cancer.

Autophagic flux induced by graphene oxide has a neuroprotective effect against human prion protein fragments.

Graphene oxide (GO) is a nanomaterial with newly developing biological applications. Autophagy is an intracellular degradation system that has been associated with the progression of neurodegenerative disorders. Although induction of autophagic flux by GO has been reported, the underlying signaling pathway in neurodegenerative disorders and how this is involved in neuroprotection remain obscure.

Hypoxia-mediated autophagic flux inhibits silver nanoparticle-triggered apoptosis in human lung cancer cells.

Solid tumors are frequently associated with resistance to chemotherapy because the fraction of hypoxic tumor cells is substantial. To understand the underlying mechanism of hypoxia on silver nanoparticle (AgNPs)-induced apoptosis, the expression of hypoxia-inducible factor (HIF)-1α, a hallmark of hypoxia, was measured in the presence and absence of AgNPs. The results showed that HIF-1α expression was upregulated after AgNPs treatment under both hypoxic and normoxic conditions.

Male- and female-derived somatic and germ cell-specific toxicity of silver nanoparticles in mouse.

Silver nanoparticles (AgNPs) are widely used as an antibiotic agent in textiles, wound dressings, medical devices, and appliances such as refrigerators and washing machines. The increasing use of AgNPs has raised concerns about their potential risks to human health. Therefore, this study was aimed to determine the impact of AgNPs in germ cell specific complications in mice.

Modulation of the expression of sphingosine 1-phosphate 2 receptors regulates the differentiation of pre-adipocytes.

Sphingosine 1-phosphate (S1P) is a bioactive lipid mediator that regulates multiple signals through S1P receptors responsible for biological responses. In particular, the S1P2 receptor has distinct roles in the S1P‑mediated differentiation of certain cell types. The present study was the first, to the best of our knowledge, to report the role of the S1P2 receptor in the adipocyte differentiation of 3T3‑L1 pre‑adipocytes.

Neuroprotective effect of cellular prion protein (PrPC) is related with activation of alpha7 nicotinic acetylcholine receptor (α7nAchR)-mediated autophagy flux.

Activation of the alpha7 nicotinic acetylcholine receptor (α7nAchR) is regulated by prion protein (PrPC) expression and has a neuroprotective effect by modulating autophagic flux. In this study, we hypothesized that PrPC may regulate α7nAchR activation and that may prevent prion-related neurodegenerative diseases by regulating autophagic flux. PrP(106-126) treatment decreased α7nAchR expression and activation of autophagic flux.

EGCG-mediated autophagy flux has a neuroprotection effect via a class III histone deacetylase in primary neuron cells.

Prion diseases caused by aggregated misfolded prion protein (PrP) are transmissible neurodegenerative disorders that occur in both humans and animals. Epigallocatechin-3-gallate (EGCG) has preventive effects on prion disease; however, the mechanisms related to preventing prion diseases are unclear. We investigated whether EGCG, the main polyphenol in green tea, prevents neuron cell damage induced by the human prion protein.

Multidimensional effects of biologically synthesized silver nanoparticles in Helicobacter pylori, Helicobacter felis, and human lung (L132) and lung carcinoma A549 cells.

Silver nanoparticles (AgNPs) are prominent group of nanomaterials and are recognized for their diverse applications in various health sectors. This study aimed to synthesize the AgNPs using the leaf extract of Artemisia princeps as a bio-reductant. Furthermore, we evaluated the multidimensional effect of the biologically synthesized AgNPs in Helicobacter pylori, Helicobacter felis, and human lung (L132) and lung carcinoma (A549) cells.

Inhibition of the autophagy flux by gingerol enhances TRAIL-induced tumor cell death.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a primary anticancer agent and a member of the tumor necrosis factor family that selectively induces apoptosis in various tumor cells, but not in normal cells. Gingerol is a major ginger component with anti-inflammatory and anti‑tumorigenic activities. Autophagy flux is the complete process of autophagy, in which the autophagosomes are lysed by lysosomes.

Melatonin regulates the autophagic flux via activation of alpha-7 nicotinic acetylcholine receptors.

Our previous study suggested that melatonin-mediated neuroprotective effects are related with the activation of autophagy. However, the mechanism of melatonin-mediated autophagic activation in prion-mediated mitochondrial damage is not reported. Alpha-7 nicotinic acetylcholine receptors (α7nAchR) is a member of nicotinic acetylcholine receptors, and α7nAchR activation regulates via melatonin.

Induction of cellular prion protein (PrPc) under hypoxia inhibits apoptosis caused by TRAIL treatment.

Hypoxia decreases cytotoxic responses to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) protein. Cellular prion protein (PrPc) is regulated by HIF-1α in neurons. We hypothesized that PrPc is involved in hypoxia-mediated resistance to TRAIL-induced apoptosis.

Pifithrin-α ameliorates resveratrol-induced two-cell block in mouse preimplantation embryos in vitro.

Treatment with resveratrol at concentrations greater than 0.5 μmol/L resulted in the arrest of mouse embryo development at the two-cell stage. Resveratrol-induced cytotoxicity was investigated in embryos by evaluating morphologic features by using the bromodeoxyuridine assay and acridine orange and ethidium bromide double staining.

Deferoxamine inhibits TRAIL-mediated apoptosis via regulation of autophagy in human colon cancer cells.

Deferoxamine (DFO), an iron chelator, has numerous clinical applications for patients presenting with iron overload in regards to the improvement in the quality of life and overall survival. In addition, experimental iron chelators have demonstrated potent anticancer properties. The present study investigated the effects of DFO on TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in colon cancer cells and and the mechanism involved.

Activation of S1P2 receptor, a possible mechanism of inhibition of adipogenic differentiation by sphingosine 1‑phosphate.

Sphingosine 1‑phosphate (S1P) belongs to a significant group of signaling sphingolipids and exerts most of its activity as a ligand of G‑protein‑coupled receptors. In our previous study, S1P demonstrated a novel biological activity with the anti‑adipogenesis of 3T3‑L1 preadipocytes. In the present study, we identified a possible mechanism of S1P‑mediated anti‑adipogenic effects, particularly in target pathways of the S1P receptors, including S1P1 and S1P2.

Evaluation of reference genes in mouse preimplantation embryos for gene expression studies using real-time quantitative RT-PCR (RT-qPCR).

Background: Real-time quantitative reverse-transcriptase polymerase chain reaction (RT-qPCR) is the most sensitive, and valuable technique for rare mRNA detection. However, the expression profiles of reference genes under different experimental conditions, such as different mouse strains, developmental stage, and culture conditions have been poorly studied.

Results: mRNA stability of the actb, gapdh, sdha, ablim, ywhaz, sptbn, h2afz, tgfb1, 18 s and wrnip genes was analyzed.

Melatonin-mediated β-catenin activation protects neuron cells against prion protein-induced neurotoxicity.

Activation of β-catenin in neurons regulates mitochondrial function and protects against protein misfolding disorders, including Alzheimer's disease and Huntington's disease. Melatonin, a natural secretory product of the pineal gland, exerts neuroprotective effects through the activation of β-catenin. In this study, melatonin increased β-catenin protein expression and activation in human neuroblastoma cell lines SH-SY5Y cells.

Oxidative stress mediated cytotoxicity of biologically synthesized silver nanoparticles in human lung epithelial adenocarcinoma cell line.

The goal of the present study was to investigate the toxicity of biologically prepared small size of silver nanoparticles in human lung epithelial adenocarcinoma cells A549. Herein, we describe a facile method for the synthesis of silver nanoparticles by treating the supernatant from a culture of Escherichia coli with silver nitrate. The formation of silver nanoparticles was characterized using various analytical techniques.

Sphingosine-1-phosphate inhibits the adipogenic differentiation of 3T3-L1 preadipocytes.

Sphingosine-1-phosphate (S1P) is a pluripotent lipid mediator that transmits signals through G-protein-coupled receptors to control diverse biological processes. The novel biological activity of S1P in the adipogenesis of 3T3-L1 preadipocytes was identified in the present study. S1P significantly decreased lipid accumulation in maturing preadipocytes in a dose‑dependent manner.

FTY720 protects neuronal cells from damage induced by human prion protein by inactivating the JNK pathway.

Prion diseases affect the central nervous system (CNS) in humans and animals, and are associated with the conversion of the cellular prion protein (PrPC) to the misfolded isoform (PrPSc). FTY720, an immune modulator and synthetic analogue of sphingosine-1-phosphate (S1P), activates S1P receptors and has been shown to be effective in experimental models of transplantation and autoimmunity, including multiple sclerosis. Whereas the immune modulatory functions of FTY720 have been extensively investigated, the other functions of FTY720 are not yet well understood.

HIF-1α-induced β-catenin activation prevents prion-mediated neurotoxicity.

Previous studies have shown that hypoxic preconditioning attenuates prion-mediated neurotoxicity by upregulating hypoxia inducible factor-1α (HIF-1α). However, the mechanisms behind the HIF-1α-mediated neuroprotective effects in neurodegenerative disorders, including prion diseases, are unclear. It is well known that HIF-1α regulates Wnt/β-catenin signaling and that β-catenin protects neurons against misfolded protein-mediated disorders, including Alzheimer's and Parkinson's disease by preventing mitochondrial malfunction.