Adipocyte enhancer binding protein 1 knockdown alleviates osteoarthritis through inhibiting NF-κB signaling pathway-mediated inflammation and extracellular matrix degradation.

Inflammation promotes the degradation of the extracellular matrix, which contributes to the development of osteoarthritis (OA). Adipocyte enhancer binding protein 1 (AEBP1) participates in multiple pathological processes related to inflammatory diseases. However, the role of AEBP1 in OA development is unknown. We found a higher AEBP1 expression in articular cartilage of OA patients (n = 20) compared to their normal controls (n = 10). Thus, we inferred that AEBP1 might affect OA progression. Then mice with destabilization of the medial meniscus (DMM) surgery and chondrocytes with IL-1ß treatment (10 ng/mL) were used to mimic OA. The increased AEBP1 expression was observed in models of OA. AEBP1 knockdown in chondrocytes reversed IL-1ß-induced inflammation and extracellular matrix degradation, which was mediated by the inactivation of NF-κB signaling pathway and the increased IκBα activity. Co-immunoprecipitation assay indicated the interaction between AEBP1 and IκBα. Importantly, IκBα knockdown depleted the protective role of AEBP1 knockdown in OA. Moreover, AEBP1 knockdown in mice with OA showed similar results to those in chondrocytes. Collectively, our findings suggest that AEBP1 knockdown alleviates the development of OA, providing a novel strategy for OA treatment.

A Critical Review on Recent Progress of Solution-Processed Monolayer Assembly of Nanomaterials and Applications.

The rapid development in nanotechnology has necessitated accurate and efficient assembly strategies for nanomaterials. Monolayer assembly of nanomaterials (MAN) represents a challenging and important architecture to manufacture and is critical in understanding interactions among nanomaterials, solvents, and substrates. MAN enables highly tunable performance in electronic and photonic devices. This review summarizes the recent progress on the methods to achieve MAN and discusses important control factors. Moreover, the importance of MAN is elaborated by a broad range of applications in electronics and photonics. In the end, the opportunities as well as challenges in manufacturing and new applications are outlooked.

MSRB2 Ameliorates H2O2-induced Chondrocyte Oxidative Stress and Suppresses Apoptosis in Osteoarthritis.

BACKGROUND: Chondrocyte oxidative stress and apoptosis are critical factors contributing to the pathogenesis of osteoarthritis (OA). Methionine sulfoxide reductase B2 (MSRB2) is a mitochondrial protein that protects cells from oxidative stress and is involved in apoptosis. This study aimed to investigated the expression of MSRB2 in articular cartilage tissues and elucidated its effect on H2O2-stimulated chondrocytes. METHODS: Human chondrocytes were cultured in Dulbecco's modified Eagle's medium (DMEM)/F12. MSRB2 overexpression in chondrocytes was achieved by transfecting with an MSRB2 overexpression plasmid. Western blot, quantitative RT-PCR, Immunofluorescence staining, and TUNEL assay were employed in this study. RESULTS: MSRB2 expression was found to be reduced in OA patients. Furthermore, overexpression of MSRB2 in H2O2-induced chondrocytes mitigated apoptosis and enhanced cell viability. Elevated MSRB2 expression diminished chondrocyte ROS contents, decreased cytochrome C (Cyc) in the cytoplasm, and regulated mitochondrial membrane potential to maintain mitochondrial homeostasis. Interestingly, knockdown of charged multivesicular body protein 5 (CHMP5) led to a decreased inMSRB2 expression in chondrocytes. Additionally, protein levels of CHMP5 and MSRB2 were reduced in H2O2-stimulated chondrocytes, and silencing CHMP5 reduced MSRB2 expression. Knockdown of CHMP5 increased cleaved caspase-3 expression in H2O2-induced chondrocytes and elevated TUNEL-positive chondrocytes. CONCLUSION: MSRB2 decreased in OA, and overexpression of MSRB2 alleviated oxidative stress and apoptosis of chondrocyte.

CHMP5 attenuates osteoarthritis via inhibiting chondrocyte apoptosis and extracellular matrix degradation: involvement of NF-κB pathway.

BACKGROUND: Osteoarthritis (OA), the most common joint disease, is linked with chondrocyte apoptosis and extracellular matrix (ECM) degradation. Charged multivesicular body protein 5 (CHMP5), a member of the multivesicular body, has been reported to serve as an anti-apoptotic protein to participate in leukemia development. However, the effects of CHMP5 on apoptosis and ECM degradation in OA remain unclear. METHODS: In this study, quantitative proteomics was performed to analyze differential proteins between normal and OA patient articular cartilages. The OA mouse model was constructed by the destabilization of the medial meniscus (DMM). In vitro, interleukin-1 beta (IL-1ß) was used to induce OA in human chondrocytes. CHMP5 overexpression and silencing vectors were created using an adenovirus system. The effects of CHMP5 on IL-1ß-induced chondrocyte apoptosis were investigated by CCK-8, flow cytometry, and western blot. The effects on ECM degradation were examined by western blot and immunofluorescence. The potential mechanism was explored by western blot and Co-IP assays. RESULTS: Downregulated CHMP5 was identified by proteomics in OA patient cartilages, which was verified in human and mouse articular cartilages. CHMP5 overexpression repressed cell apoptosis and ECM degradation in OA chondrocytes. However, silencing CHMP5 exacerbated OA chondrocyte apoptosis and ECM degradation. Furthermore, we found that the protective effect of CHMP5 against OA was involved in nuclear factor kappa B (NF-κB) signaling pathway. CONCLUSIONS: This study demonstrated that CHMP5 repressed IL-1ß-induced chondrocyte apoptosis and ECM degradation and blocked NF-κB activation. It was shown that CHMP5 might be a novel potential therapeutic target for OA in the future.

Engineering chirality at wafer scale with ordered carbon nanotube architectures.

Creating artificial matter with controllable chirality in a simple and scalable manner brings new opportunities to diverse areas. Here we show two such methods based on controlled vacuum filtration - twist stacking and mechanical rotation - for fabricating wafer-scale chiral architectures of ordered carbon nanotubes (CNTs) with tunable and large circular dichroism (CD). By controlling the stacking angle and handedness in the twist-stacking approach, we maximize the CD response and achieve a high deep-ultraviolet ellipticity of 40 ± 1 mdeg nm-1. Our theoretical simulations using the transfer matrix method reproduce the experimentally observed CD spectra and further predict that an optimized film of twist-stacked CNTs can exhibit an ellipticity as high as 150 mdeg nm-1, corresponding to a g factor of 0.22. Furthermore, the mechanical rotation method not only accelerates the fabrication of twisted structures but also produces both chiralities simultaneously in a single sample, in a single run, and in a controllable manner. The created wafer-scale objects represent an alternative type of synthetic chiral matter consisting of ordered quantum wires whose macroscopic properties are governed by nanoscopic electronic signatures and can be used to explore chiral phenomena and develop chiral photonic and optoelectronic devices.

HGFIN deficiency exacerbates spinal cord injury by promoting inflammation and cell apoptosis through regulation of the PI3K/AKT signaling pathway.

BACKGROUND: Spinal cord injury (SCI) is a devastating neurological disease characterized by neuroinflammation and neuronal apoptosis. The PI3K/AKT signaling pathway is related to the pathological process of SCI. Hematopoietic growth factor inducible neurokinin-1 type (HGFIN) is a transmembrane glycoprotein that exerts neuroprotective actions in various neurodegenerative diseases. However, the potential role and mechanism of HGFIN in the development of SCI are still unclear. OBJECTIVES: To investigate the effect of HGFIN on inflammation and neuronal apoptosis as well as the underlying mechanism in SCI. MATERIAL AND METHODS: A rat model of SCI was established, and Basso-Beattie-Bresnahan (BBB) motor function assay was performed to detect motor function. Expression of HGFIN was measured at 7 days after injury by western blot and immunofluorescence. An HGFIN-shRNA-carrying lentivirus was injected into the injury site to block the expression of HGFIN. The effects of HGFIN on neuronal apoptosis and the PI3K/AKT pathway were analyzed by TUNEL staining and immunofluorescence. The Iba-1 expression and the levels of pro-inflammatory cytokines were measured in spinal cord tissues by immunofluorescence staining and real-time polymerase chain reaction (PCR) analysis. RESULTS: The SCI rats showed increased expression of HGFIN in spinal cord tissues. The HGFIN deficiency aggravated SCI lesions, as evidenced by decreased BBB scores. At 7 days post-injury, HGFIN knockdown promoted neuronal apoptosis, accompanied by the increased expression level of the apoptosis effector cleaved caspase-3 and cleaved PARP, and decreased anti-apoptotic protein Bcl-2 expression. Moreover, HGFIN knockdown aggravated the inflammation process, indicated by increased Iba1-positive cells. The HGFIN knockdown increased the production of pro-inflammatory cytokines including IL-1ß, TNF-α and IL-6. Further analysis revealed that HGFIN deficiency reduced the activation of the PI3K/AKT pathway in spinal cord tissue after injury. CONCLUSIONS: Lentivirus-mediated downregulation of HGFIN exacerbates inflammation and neuronal apoptosis in SCI by regulating the PI3K/AKT pathway, and provides clues for developing novel therapeutic approaches and targets against SCI.

SNIP1 reduces extracellular matrix degradation and inflammation via inhibiting the NF-κB signaling pathway in osteoarthritis.

Osteoarthritis (OA), the most common joint disease, is characterized by inflammation and cartilage degradation. Previous studies illustrated that Smad nuclear-interacting protein 1 (SNIP1) is an inhibitor of the TGF-ß signal transduction pathway and SNIP1 has been reported as an anti-inflammatory factor. This study aimed to explore the role of SNIP1 in OA progression. In this study, the SNIP1 expression was evaluated in OA human and OA mice tissue and interleukin-1 beta (IL-1ß)-induced chondrocytes. The Safranin-O (SO) staining and osteoarthritis research society international (OARSI) scoring system was used to evaluate cartilage injury. The gain- and loss-of-function studies for SNIP1 were performed in chondrocytes. The SNIP1 overexpression adenovirus was injected into mice by intra-articular injection. The SNIP1 expression was decreased in OA patients, OA mice, and IL-1ß-stimulated chondrocytes. The cartilage injury of medial meniscus-induced OA (DMM-OA) mice at 8 weeks showed more severe than that at 4 weeks. The expression of SNIP1 was lower at 8 weeks than that at 4 weeks. In IL-1ß-stimulated chondrocytes, SNIP1 overexpression reduced the expression of TNF-α and IL-6, alleviated ECM degradation, reduced the phosphorylation levels of p65 and IκBα, and decreased the p65 level in nuclear. Moreover, overexpression of SNIP1 alleviated cartilage injury in DMM-OA mice. In brief, our study suggested that SNIP1 alleviated OA and repressed inflammation by inhibiting the activation of NF-κB. This study might provide a new insight into OA treatment.

Exercise in cold: Friend than foe to cardiovascular health.

Exercise has been proven to benefit human health comprehensively regardless of the intensity, time, or environment. Recent studies have found that combined exercise with a cold environment displays a synergistical beneficial effect on cardiovascular system compared to exercise in thermoneutral environment. Cold environment leads to an increase in body heat loss, and has been considered a notorious factor for cardiovascular system. Exercise in cold increases the stress of cardiovascular system and risks of cardiovascular diseases, but increases the body tolerance to detrimental insults and benefits cardiovascular health. The biological effects and its underlying mechanisms of exercise in cold are complex and not well studied. Evidence has shown that exercise in cold exerts more noticeable effects on sympathetic nervous activation, bioenergetics, anti-oxidative capacity, and immune response compared to exercise in thermoneutral environment. It also increases the secretion of a series of exerkines, including irisin and fibroblast growth factor 21, which may contribute to the cardiovascular benefits induced by exercise in cold. Further well-designed studies are needed to advance the biological effects of exercise in cold. Understanding the mechanisms underlying the benefits of exercise in cold will help prescribe cold exercise to those who can benefit from it.

BASP1 knockdown suppresses chondrocyte apoptosis and extracellular matrix degradation in vivo and in vitro: A possible therapeutic approach for osteoarthritis.

Osteoarthritis(OA) is an age-related degenerative disease involving chondrocyte apoptosis and extracellular matrix(ECM) degradation.Brain acid soluble protein 1(BASP1) has been reported to induce apoptosis.Thus, we speculated that BASP1 might regulate OA progression by inducing apoptosis, which is also the purpose of this study.The cartilage of the knee joint was collected from OA patients who received the joint replacement.In OA cartilage tissue,we found BASP1 expression was highly expressed, which inferred that BASP1 might be involved in OA.To validate our hypothesis, destabilization of the medial meniscus (DMM) surgery-induced male C57BL/6mice and interleukin-1ß (IL-1ß)-treated human chondrocytes were used to mimic the OA environment.BASP1 knockdown in mice and chondrocytes was achieved by adenovirus carried with BASP1-specific shRNA.High expression of BASP1 was observed in OA mice, which was also verified in IL-1ß-treated chondrocytes.The potential mechanism of BASP1 in OA was further explored in vitro.BASP1 knockdown alleviated IL-1ß-induced apoptosis and ECM degradation, as reflected by the decreased number of apoptotic cells and matrix metalloproteases 13 expression,and the increased collagen II expression.Our findings indicated that BASP1 knockdown alleviated OA progression by inhibiting apoptosis and ECM degradation, suggesting that inhibiting BASP1 may be a potentially applicable method for preventing OA.

Transition from Diffusive to Superdiffusive Transport in Carbon Nanotube Networks via Nematic Order Control.

The one-dimensional confinement of quasiparticles in individual carbon nanotubes (CNTs) leads to extremely anisotropic electronic and optical properties. In a macroscopic ensemble of randomly oriented CNTs, this anisotropy disappears together with other properties that make them attractive for certain device applications. The question however remains if not only anisotropy but also other types of behaviors are suppressed by disorder. Here, we compare the dynamics of quasiparticles under strong electric fields in aligned and random CNT networks using a combination of terahertz emission and photocurrent experiments and out-of-equilibrium numerical simulations. We find that the degree of alignment strongly influences the excited quasiparticles' dynamics, rerouting the thermalization pathways. This is, in particular, evidenced in the high-energy, high-momentum electronic population (probed through the formation of low energy excitons via exciton impact ionization) and the transport regime evolving from diffusive to superdiffusive.

Phonon-Assisted Intertube Electronic Transport in an Armchair Carbon Nanotube Film.

The electrical conductivity of a macroscopic assembly of nanomaterials is determined through a complex interplay of electronic transport within and between constituent nano-objects. Phonons play dual roles in this situation: their increased populations tend to reduce the conductivity via electron scattering, while they can boost the conductivity by assisting electrons to propagate through the potential-energy landscape. We identified a phonon-assisted coherent electron transport process between neighboring nanotubes in temperature-dependent conductivity measurements on a macroscopic film of armchair single-wall carbon nanotubes. Through atomistic modeling of electronic states and calculations of both electronic and phonon-assisted junction conductances, we conclude that phonon-assisted conductance is the dominant mechanism for observed high-temperature transport in armchair carbon nanotubes. The unambiguous manifestation of coherent intertube dynamics proves a single-chirality armchair nanotube film to be a unique macroscopic solid-state ensemble of nano-objects promising for the development of room-temperature coherent electronic devices.

Effects of interlayer reflection and interpixel interaction in diffractive optical neural networks.

Multilayer diffractive optical neural networks (DONNs) can perform machine learning (ML) tasks at the speed of light with low energy consumption. Decreasing the number of diffractive layers can reduce inevitable material and diffraction losses to improve system performance, and incorporating compact devices can reduce the system footprint. However, current analytical DONN models cannot accurately describe such physical systems. Here we show the ever-ignored effects of interlayer reflection and interpixel interaction on the deployment performance of DONNs through full-wave electromagnetic simulations and terahertz (THz) experiments. We demonstrate that the drop of handwritten digit classification accuracy due to reflection is negligible with conventional low-index THz polymer materials, while it can be substantial with high-index materials. We further show that one- and few-layer DONN systems can achieve high classification accuracy, but there is a trade-off between accuracy and model-system matching rate because of the fast-varying spatial distribution of optical responses in diffractive masks. Deep DONNs can break down such a trade-off because of reduced mask spatial complexity. Our results suggest that new accurate and trainable DONN models are needed to advance the development and deployment of compact DONN systems for sophisticated ML tasks.

3,3'-diindolylmethane inhibits LPS-induced human chondrocytes apoptosis and extracellular matrix degradation by activating PI3K-Akt-mTOR-mediated autophagy.

Osteoarthritis (OA) is a chronic degenerative joint disease characterized by articular cartilage destruction. The pathological mechanisms are complex; in particular, inflammation, autophagy, and apoptosis are often involved. 3,3-Diindolylmethane (DIM), a phytoconstituent extracted from cruciferous vegetables, has various effects such as anti-inflammatory, antioxidant and anti-apoptotic. However, the effects of DIM on osteoarthritic chondrocytes remain undetermined. In this study, we simulated a lipopolysaccharide (LPS)-induced osteoarthritis model in human primary chondrocytes. We found that LPS stimulation significantly inhibited autophagy, induced chondrocyte apoptosis and extracellular matrix (ECM) degradation, which could be ameliorated by DIM. DIM inhibited the expression of a disintegrin and metalloproteinase with thrombospondin motif 5 (ADAMTS-5), matrix metalloproteinase 13 (MMP13), cleaved caspase-3, Bax, and p62, and increased the expression level of collagen II, aggrecan, Bcl-2, light chain 3 Ⅱ (LC3 Ⅱ), and beclin-1. Mechanistic studies showed that DIM increased chondrocyte autophagy levels by inhibiting the activation of PI3K/AKT/mTOR pathway. In mice destabilization of the medial meniscus (DMM) model, immunohistochemical analysis showed that DIM inhibited the expression of p-PI3K and cleaved caspase-3, increased the expression of LC3 Ⅱ. Furthermore, DIM relieved joint cartilage degeneration. In conclusion, our findings demonstrate for the first time that DIM inhibits LPS-induced chondrocyte apoptosis and ECM degradation by regulating the PI3K/AKT/mTOR-autophagy axis and delays OA progression in vivo.

Wafer-Scale Full-Coverage Self-Limiting Assembly of Particles on Flexible Substrates.

Self-limiting assembly of particles represents the state-of-the-art controllability in nanomanufacturing processes where the assembly stops at a designated stage, providing a desirable platform for applications requiring delicate thickness control such as optics, electronics, and catalytic systems. Most successes in self-limiting assembly are limited to self-assembled monolayers (SAMs) of small molecules on inorganic, chemically homogeneous rigid substrates (e.g., Au and SiO2) through surface-interaction mechanisms. Similar mechanisms, however, cannot achieve a uniform assembly of particles on flexible polymer substrates. The complex configurations and conformations of polymer chains create a surface with nonuniform distributions of chemical groups and phases. In addition, most assembly mechanisms require good solvent wettability, where many desirable but hard-to-wet particles and polymer substrates are excluded. Here, we demonstrate a collision-based self-limiting assembly (CSA) to achieve wafer-scale, full-coverage, close-packed monolayers of hydrophobic particles on hydrophobic polymer substrates in aqueous solutions. The kinetic assembly and self-limiting processes are facilitated and controlled by the combined acoustic and shear fields. We envision many applications in functional coatings and showcase their feasibility in structural coloration. Importantly, such functional coatings can be repaired using CSA, and both particles and polymer substrate can be recycled.

Graphene plasmonic spatial light modulator for reconfigurable diffractive optical neural networks.

Terahertz (THz) diffractive optical neural networks (DONNs) highlight a new route toward intelligent THz imaging, where the image capture and classification happen simultaneously. However, the state-of-the-art implementation mostly relies on passive components and thus the functionalities are limited. The reconfigurability can be achieved through spatial light modulators (SLMs), while it is not clear what device specifications are required and how challenging the associated device implementation is. Here, we show that a complex-valued modulation with a π/2 phase modulation in an active reflective graphene-plasmonics-based SLM can be employed for realizing the reconfigurability in THz DONNs. By coupling the plasmonic resonance in graphene nanoribbons with the reflected Fabry-Pérot (F-P) mode from a back reflector, we achieve a minor amplitude modulation of large reflection and a substantial π/2 phase modulation. Furthermore, the constructed reconfigurable reflective THz DONNs consisting of designed SLMs demonstrate >94.0% validation accuracy of the MNIST dataset. The results suggest that the relaxation of requirements on the specifications of SLMs should significantly simplify and enable varieties of SLM designs for versatile DONN functionalities.

Carbon Nanotube Devices for Quantum Technology.

Carbon nanotubes, quintessentially one-dimensional quantum objects, possess a variety of electrical, optical, and mechanical properties that are suited for developing devices that operate on quantum mechanical principles. The states of one-dimensional electrons, excitons, and phonons in carbon nanotubes with exceptionally large quantization energies are promising for high-operating-temperature quantum devices. Here, we discuss recent progress in the development of carbon-nanotube-based devices for quantum technology, i.e., quantum mechanical strategies for revolutionizing computation, sensing, and communication. We cover fundamental properties of carbon nanotubes, their growth and purification methods, and methodologies for assembling them into architectures of ordered nanotubes that manifest macroscopic quantum properties. Most importantly, recent developments and proposals for quantum information processing devices based on individual and assembled nanotubes are reviewed.

Shikonin, a promising therapeutic drug for osteoarthritis that acts via autophagy activation.

Osteoarthritis (OA) is a chronic joint degenerative disease characterised by narrowed articular space, formation of surrounding osteophytes, and subchondral bone sclerosis. OA is caused by cartilage degeneration, which is closely correlated with the disequilibrium of anabolism and catabolism in chondrocytes. Previous studies have revealed that autophagy plays a significant role in maintaining the balance of anabolic and catabolic activities. Thus, targeting autophagy may be a promising therapeutic strategy for OA. Shikonin, a traditional Chinese herbal medicine isolated from flavonoid glucuronide, has drawn focus for its role in activating autophagy. In this study, the mRNA and protein level of a disintegrin and metalloproteinase with thrombospondin motifs-5 and matrix metalloproteinases-1 decreased with shikonin treatment, in the IL-1ß-induced OA cell model. On the contrary, IL-1ß-induced downregulation of Aggrecan and Collagen II was ameliorated following shikonin treatment. In addition, the upregulation of autophagy-related marker genes Beclin-1 and LC3II/LC3I in chondrocytes indicated that autophagy could be activated upon shikonin treatment. Moreover, shikonin's promotion of anabolism in chondrocytes through autophagy activation corresponded with the results from the examination using chloroquine, an autophagy inhibitor. OA mouse cartilage tissues were stained with safranin O and fast green dyes. Results were analysed using the Osteoarthritis Research Society International (OARSI) score, and suggested that mice cartilage degeneration was alleviated after shikonin treatment. Altogether, we identified that shikonin might be a novel promising drug for OA treatment.

Hall effect in gated single-wall carbon nanotube films.

The presence of hopping carriers and grain boundaries can sometimes lead to anomalous carrier types and density overestimation in Hall-effect measurements. Previous Hall-effect studies on carbon nanotube films reported unreasonably large carrier densities without independent assessments of the carrier types and densities. Here, we have systematically investigated the validity of Hall-effect results for a series of metallic, semiconducting, and metal-semiconductor-mixed single-wall carbon nanotube films. With carrier densities controlled through applied gate voltages, we were able to observe the Hall effect both in the n- and p-type regions, detecting opposite signs in the Hall coefficient. By comparing the obtained carrier types and densities against values derived from simultaneous field-effect-transistor measurements, we found that, while the Hall carrier types were always correct, the Hall carrier densities were overestimated by up to four orders of magnitude. This significant overestimation indicates that thin films of one-dimensional SWCNTs are quite different from conventional hopping transport systems.

Physics-informed recurrent neural network for time dynamics in optical resonances.

Resonance structures and features are ubiquitous in optical science. However, capturing their time dynamics in real-world scenarios suffers from long data acquisition time and low analysis accuracy due to slow convergence and limited time windows. Here we report a physics-informed recurrent neural network to forecast the time-domain response of optical resonances and infer corresponding resonance frequencies by acquiring a fraction of the sequence as input. The model is trained in a two-step multi-fidelity framework for high-accuracy forecast, using first a large amount of low-fidelity physical-model-generated synthetic data and then a small set of high-fidelity application-specific data. Through simulations and experiments, we demonstrate that the model is applicable to a wide range of resonances, including dielectric metasurfaces, graphene plasmonics and ultra-strongly coupled Landau polaritons, where our model captures small signal features and learns physical quantities. The demonstrated machine-learning algorithm can help to accelerate the exploration of physical phenomena and device design under resonance-enhanced light-matter interaction.

TNF-α up-regulates Nanog by activating NF-κB pathway to induce primary rat spinal cord astrocytes dedifferentiation.

AIMS: Astrocytes re-acquire stem cell potential upon inflammation, thereby becoming a promising source of cells for regenerative medicine. Nanog is an essential transcription factor to maintain the characteristics of stem cells. We aimed to investigate the role of Nanog in astrocyte dedifferentiation. MAIN METHODS: TNF-α was used to induce the dedifferentiation of primary rat spinal cord astrocytes. The expression of immature markers CD44 and Musashi-1 was detected by qRT-PCR and immunofluorescence. The Nanog gene is knocked down by small interference RNA. Nanog expression was measured by qRT-PCR and western blotting. BAY 11-7082 was used to suppress NF-κB signals in astrocytes. NF-κB signaling was evaluated by Western blotting. KEY FINDINGS: Our results showed that TNF-α promoted the re-expression of CD44 and Musashi-1 in astrocytes. Dedifferentiated astrocytes could be induced to differentiate into oligodendrocyte lineage cells indicating that the astrocytes had pluripotency. In addition, TNF-α treatment activated NF-κB signaling pathway and up-regulated Nanog. Knockdown of Nanog reversed the increase of CD44 and Musashi-1 induced by TNF-α without affecting the activation of NF-κB signaling. Importantly, blocking NF-κB signaling by BAY 11-7082 inhibited the expression of immature markers suggesting that TNF-α induces dedifferentiation of astrocytes through the NF-κB signaling pathway. BAY 11-7082 could also inhibit the expression of Nanog, which indicated that Nanog was regulated by NF-κB signaling pathway. SIGNIFICANCE: These findings indicate that activation of the NF-κB signaling pathway through TNF-α leads to astrocytes dedifferentiation via Nanog. These results expand our understanding of the mechanism of astrocytes dedifferentiation.