Role of electron localisation in H adsorption and hydride formation in the Mg basal plane under aqueous corrosion: a first-principles study.

Understanding hydrogen-metal interactions is important in various fields of surface science, including the aqueous corrosion of metals. The interaction between atomic H and a Mg surface is a key process for the formation of sub-surface Mg hydride, which may play an important role in Mg aqueous corrosion. In the present work, we performed first-principles Density Functional Theory (DFT) calculations to study the mechanisms for hydrogen adsorption and crystalline Mg hydride formation under aqueous conditions. The Electron Localisation Function (ELF) is found to be a promising indicator for predicting stable H adsorption in the Mg surface. It is found that H adsorption and hydride layer formation is dominated by high ELF adsorption sites. Our calculations suggest that the on-surface adsorption of atomic H, OH radicals and atomic O could enhance the electron localisation at specific sites in the sub-surface region, thus forming effective H traps locally. This is predicted to result in the formation of a thermodynamically stable sub-surface hydride layer, which is a potential precursor of the crucial hydride corrosion product of magnesium.

Ubiquitin-Specific Peptidase 10 (USP10) Inhibits Hepatic Steatosis, Insulin Resistance, and Inflammation Through Sirt6.

Nonalcoholic fatty liver disease (NAFLD) is characterized by hepatic steatosis, insulin resistance and inflammation, and the pathogenic mechanism of NAFLD is poorly understood. Ubiquitin-specific peptidase 10 (USP10), a member of the ubiquitin-specific protease family, is involved in environmental stress responses, tumor growth, inflammation, and cellular metabolism. However, the role of USP10 in hepatic steatosis, insulin resistance, and inflammation remains largely unexplored. USP10 expression was detected in livers of patients with NAFLD, mice with high-fat diet (HFD)-induced obesity, and genetically obese (ob/ob) mice, as well as in palmitate-induced hepatocytes. The function of USP10 in hepatic steatosis, insulin resistance, and inflammation was investigated using hepatocyte-specific USP10 deficiency or overexpression in mice induced by HFD treatment or genetic defect. The molecular mechanisms underlying USP10-regulated hepatic steatosis were further investigated in HFD-treated mice. USP10 expression was significantly decreased in the fatty livers of NAFLD patients and obese mice and in palmitate-treated hepatocytes. USP10 deficiency exacerbated the metabolic dysfunction induced by HFD treatment for 12 weeks. Conversely, USP10 overexpression significantly suppressed metabolic dysfunction in mice after HFD treatment and inhibited the development of NAFLD in ob/ob mice. Further investigation indicated that USP10 regulates hepatic steatosis by interacting with Sirt6 and inhibiting its ubiquitination and degradation. Sirt6 overexpression markedly ameliorated the effects of USP10 deficiency in hepatic steatosis, insulin resistance, and inflammation. Conversely, Sirt6 deficiency decreased the ameliorative effects of USP10 overexpression in response to HFD treatment. Conclusion: USP10 inhibits hepatic steatosis, insulin resistance, and inflammation through Sirt6.

MALAT1 Promotes Cell Apoptosis and Suppresses Cell Proliferation in Testicular Ischemia-Reperfusion Injury by Sponging MiR-214 to Modulate TRPV4 Expression.

BACKGROUND/AIMS: Accumulating evidences has indicated that aberrant expression of long non-coding RNAs (lncRNAs) is tightly associated with the progression of ischemia-reperfusion injury (IRI). Previous studies have reported that lncRNA MALAT1 regulates cell apoptosis and proliferation in myocardial and cerebral IRI. However, the underlying mechanism of MALAT1 in testicular IRI has not been elucidated. METHODS: The levels of MALAT1, some related proteins and apoptosis in the testicular tissues were determined by quantitative real-time PCR, HE staining, immunohistochemistry, western blot and TUNEL assays. Relative expression of MALAT1, miR-214 and related proteins in cells were measured by western blot and quantitative real-time PCR. Cell viability and apoptosis were examined using MTT assay and flow cytometry. RESULTS: In the present study, we found that MALAT1 was up-regulated in animal samples and GC-1 cells. The expression level of MALAT1 was positively related to cell apoptosis and negatively correlated with cell proliferation as testicular IRI progressed. In gain and loss of function assays, we confirmed that MALAT1 promotes cell apoptosis and suppresses cell proliferation in vitro and in vivo. Furthermore, we found that MALAT1 negatively regulates expression of miR-214 and promotes TRPV4 expression at the post-transcriptional level. Consequently, we investigated the correlation between MALAT1 and miR-214 and identified miR-214 as a direct target of MALAT1. In addition, we found that TRPV4 acted as a target of miR-214. Over-expression of miR-214 efficiently abrogated the up-regulation of TRPV4 induced by MALAT1, suggesting that MALAT1 positively regulates the expression of TRPV4 by sponging miR-214. CONCLUSION: In sum, our study indicated that the lncRNA MALAT1 promotes cell apoptosis and suppresses cell proliferation in testicular IRI via miR-214 and TRPV4.

Tisp40 deficiency attenuates renal ischemia reperfusion injury induced apoptosis of tubular epithelial cells.

Renal ischemia reperfusion (IR) is a major cause of acute kidney injury (AKI) and no effective treatments have been established. Tisp40 is a transcription factor of the CREB/ATF family and involves in cell apoptosis, proliferation and differentiation, but its role in renal IR remains unknown. Here, we investigated the role of Tisp40 in renal IR injury. In vivo, Tisp40 knockout (KO) and wild-type (WT) mice were subjected to thirty minutes of bilateral renal ischemia and 48h reperfusion, the blood and kidneys were harvested for analysis. In vitro, Tisp40 overexpression and vector cells were subjected to hypoxia/reoxygenation (HR), the apoptosis rate and the expressions of related proteins were measured. Following IR, the expressions of Tisp40 protein, serum creatinine (sCr), blood urea nitrogen (BUN) and apoptosis of tubular cells were significantly increased in WT mice. However, Tisp40 deficiency significantly attenuated the increase of sCr, BUN and apoptosis of tubular cells. Following HR, apoptosis of tubular cells was increased in Tisp40 overexpression cells compared with vector cells. Mechanistically, Tisp40 promoted the expressions of C/EBP homologous protein (CHOP), Bax and Cleaved caspase3 and suppressed the expression of Bcl-2 in renal IR injury. In conclusion, Tisp40 aggravates tubular cells apoptosis in renal IR injury.

MiR-543 Promotes Proliferation and Epithelial-Mesenchymal Transition in Prostate Cancer via Targeting RKIP.

BACKGROUND/AIMS: MicroRNAs (miRNAs, miRs) have emerged as important post-transcriptional regulators in various cancers. miR-543 has been reported to play critical roles in hepatocellular carcinoma and colorectal cancer, however, the role of miR-543 in the pathogenesis of prostate cancer has not been fully understood. METHODS: Expression of miR-543 and Raf Kinase Inhibitory Protein (RKIP) in clinical prostate cancer specimens, two prostate cancer cell lines, namely LNCAP and C4-2B, were determined. The effects of miR-543 on proliferation and metastasis of tumor cells were also investigated with both in vitro and in vivo studies. RESULTS: miR-543 was found to be negatively correlated with RKIP expression in clinical tumor samples and was significantly upregulated in metastatic prostate cancer cell line C4-2B compared with parental LNCAP cells. Further studies identified RKIP as a direct target of miR-543. Overexpression of miR-543 downregulated RKIP expression and promoted the proliferation and metastasis of cancer cells, whereas knockdown of miR-543 increased expression of RKIP and suppressed the proliferation and metastasis of cancer cells in vitro and in vivo. CONCLUSION: Our study demonstrates that miR-543 promotes the proliferation and metastasis of prostate cancer via targeting RKIP.

Identification of Tisp40 as an Essential Regulator of Renal Tubulointerstitial Fibrosis via TGF-ß/Smads Pathway.

BACKGROUND: Tisp40, a transcription factor of the CREB/CREM family, is involved in cell proliferation, differentiation and other biological functions, but its role in renal tubulointerstitial fibrosis is unknown. METHODS: In our study, we investigated the effects of Tisp40 on extracellular matrix (ECM) accumulation, epithelial-mesenchymal transition (EMT) and the underlying molecular mechanisms in transforming growth factor-ß (TGF-ß)-stimulated TCMK-1 cells by quantitative real-time polymerase chain reaction (qPCR), Western blot analysis and immunofluorescence in vitro, and further explored the role of Tisp40 on renal fibrosis induced by ischemia-reperfusion (I/R) by qPCR, Western blot analysis, hydroxyproline analysis, Masson trichrome staining and immunohistochemistry staining in vivo. RESULTS: The data showed that Tisp40 was upregulated in a model of renal fibrosis induced by I/R injury (IRI). Upon IRI, Tisp40-deficient mice showed attenuated renal fibrosis compared with wild-type mice. Furthermore, the expression of α-smooth muscle actin, E-cadherin, fibronectin, and collagen I was suppressed. Tisp40 overexpression aggravated ECM accumulation and EMT in the TGF-ß-stimulated TCMK-1 cell line, whereas the opposite occurred in cells treated with small interfering RNA (siRNA) targeting Tisp40. Importantly, it is changes in the Smad pathway that attenuate renal fibrosis. CONCLUSION: These findings suggest that Tisp40 plays a critical role in the TGF-ß/ Smads pathway involved in this process. Hence, Tisp40 could be a useful therapeutic target in the fight against renal tubulointerstitial fibrosis.

Corrigendum: Identification of microRNA-92a-3p as an essential regulator of tubular epithelial cell pyroptosis by targeting Nrf1 via HO-1.

[This corrects the article DOI: 10.3389/fgene.2020.616947.].

[GC-MS analysis of chemical constituents of essential oil from Callicarpa kwangtungensis and their antimicrobial activity].

OBJECTIVE: To analyze the chemical constituents of the essential oil from Callicarpa kwangtungensis and investigate their antimicrobial activity in vitro. METHODS: The essential oil of Callicarpa kwangtungensis were extracted by steam distillaton. The chemical constituents were separated and analyzed by GC-MS. Their relative percentages were calculated with peak area normalization method. RESULTS: 38 compounds were identified, accounting for 76.01% of the peak area of the total ion-current chromatogram. The essential oil had different antimicrobial activities. CONCLUSION: The main constituent of the essential oil is terpenoids (59.25%), and showing different activities against Staphylococcus aureus, Escherichia coli and Candida albicans.

MicroRNA-214-3p aggravates ferroptosis by targeting GPX4 in cisplatin-induced acute kidney injury.

Acute kidney injury (AKI) induced by cisplatin (cis-AKI) involves indicators such as inflammation and oxidative stress (OS) in proximal tubules, although its underlying mechanisms remain largely unknown so far. Exploration of the molecular mechanisms underlying cisplatin-induced AKI is of great significance for AKI prevention and also for preventing its progression into chronic kidney disease (CKD) or end-stage renal disease (ESRD). OS and ferroptosis are mutually causal; they finally lead to the regulatory cell injury and death induced by the accumulation of reactive oxygen species (ROS). GPX4 is critical not only in OS, but studies established as the key regulator of ferroptosis. In this context, the present study focused on determining the biological function of miR-214-3p in the cisplatin-induced ferroptosis of tubular epithelial cell (TEC) and the underlying molecular mechanism. The relationship between TEC ferroptosis and cisplatin-induced AKI was investigated in vitro and in vivo. Ferrostatin-1(Fer-1), an inhibitor of ferroptosis, was observed to confer a protective effect against the renal tubular injury and renal failure induced by cisplatin. MicroRNAs (miRNAs) regulate the genes that have important functions in the development of cis-AKI. In the present study, GPX4 was predicted as a target of miR-214-3p. Moreover, inhibiting miR-214-3p enhanced the expressions of GPX4 and SLC7A11 while decreasing the ACSL4 expression. Furthermore, miR-214-3p down-regulation protected against TEC death and renal tubule damage both in vitro and in vivo. According to these findings, inhibiting miR-214-3p would alleviate TEC ferroptosis in cis-AKI via GPX4.

Establishment of two new Anaplecta species (Blattodea, Blattoidea, Anaplectidae) based on morphological and COI data with an additional description of Anaplectafurcata Deng & Che, 2020.

Based on morphological characteristics, including male and female genitalia, combined with DNA barcodes, two new species, Anaplectacircinalis Deng & Che, sp. nov. and Anaplectabihamata Deng & Che, sp. nov., are described in detail. Additional information on the female genitalia of Anaplectafurcata Deng & Che, 2020 is also provided. Photographs of external morphology and caudal anatomy of these species, as well as a key to the Chinese Anaplecta species, are provided.

Unraveling the Role of Architecture in Polymer-Based Glues for Hydrogels.

We investigate polymers of different architectures as potential candidates for the development of glues for hydrogels. Using a combination of coarse-grained modeling and molecular dynamics simulations, we systematically characterize the link between experimentally tunable parameters and adhesion energy. We find that, for a broad set of parameters, adhesion is controlled almost exclusively by the total amount of glue at the interface and by the glue-hydrogel affinity. Instead, it is largely independent of changes in polymer architecture and size, a conclusion that shines new light on previously observed experimental trends. Additionally, we show that the scaling behavior of the properties we measure can be explained by modeling the glue as an ensemble of ideal, noninteracting, and linear polymer segments. We expect that the fundamental insights herein provided will aid the design of new polymer-based adhesives for hydrogels.

Effect of miR-183-5p on Cholestatic Liver Fibrosis by Regulating Fork Head Box Protein O1 Expression.

Liver fibrosis is a common pathological feature of end-stage liver disease and has no effective treatment. MicroRNAs (miRNAs) have been found to modulate gene expression in liver disease. But the potential role of miRNA in hepatic fibrosis is still unclear. The objective of this research is to study the potential mechanism and biological function of miR-183-5p in liver fibrosis. In this study, we used high-throughput sequencing to find that miR-183-5p is upregulated in human fibrotic liver tissues. In addition, miR-183-5p was upregulated both in rat liver fibrosis tissue induced by bile-duct ligation (BDL) and activated LX-2 cells (human hepatic stellate cell line) according to the result of quantitative real-time PCR (RT-qPCR). Moreover, the inhibition of miR-183-5p alleviated liver fibrosis, decreased the fibrotic biomarker levels in vitro and in vivo, and led toLX-2 cell proliferation inhibition and, apoptosis induction. The result of dual-luciferase assay revealed that miR-183-5p suppressed fork head box protein O1 (FOXO1) expression by binding to its 3'UTR directly. Next, we used lentivirus to overexpress FOXO1 in LX-2 cells, and we found that overexpression of FOXO1 reversed the promotion of miR-183-5p on liver fibrosis, reducing the fibrotic biomarker levels inLX-2 cells, inhibitingLX-2 cell proliferation, and promoting apoptosis. Furthermore, overexpression of FOXO1 prevented the activation of the transforming growth factor (TGF)-ß signaling pathway in TGF-ß1-induced LX-2 cells according to the result of western blotting. In conclusion, the findings showed thatmiR-183-5p might act as a key regulator of liver fibrosis, and miR-183-5p could promote cholestatic liver fibrosis by inhibiting FOXO1 expression through the TGF-ß signaling pathway. Thus, inhibition of miR-183-5pmay be a new way to prevent and improve liver fibrosis.

Coexistence of Ferroelectricity and Ferromagnetism in One-Dimensional SbN and BiN Nanowires.

Ferroelectricity exists in a variety of three- and two-dimensional materials and is of great significance for the development of electronic devices. However, the presence of ferroelectricity in one-dimensional materials is extremely rare. Here, we predict ferroelectricity in one-dimensional SbN and BiN nanowires. Their polarization strengths are 1 order of magnitude higher than ever reported values in one-dimensional structures. Moreover, we find that spontaneous spin polarization can be generated in SbN and BiN nanowires by moderate hole doping. This is the first time the coexistence of both ferroelectricity and ferromagnetism in a one-dimensional system has been reported. Our finding not only broadens the family of one-dimensional ferroelectric materials but also offers a promising platform for novel electronic and spintronic applications.

Tisp40 Induces Tubular Epithelial Cell GSDMD-Mediated Pyroptosis in Renal Ischemia-Reperfusion Injury via NF-κB Signaling.

Renal ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury (AKI). As a transcription factor, the Transcript induced in spermiogenesis 40 (Tisp40) has been found to be involved in renal IRI. However, the role of Tisp40 in tubular epithelial cell (TEC) pyroptosis of renal IRI remains unknown. In this study, we investigated effects of Tisp40 on Gasdermin D (GSDMD)-mediated TEC pyroptosis in renal IRI and underlying molecular mechanisms in I/R-induced kidney by hematoxylin and eosin (HE) staining, Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay,immunohistochemistry (IHC), reverse transcription-quantitative PCR (RT-qPCR) and western blot analysis in vivo and oxygen-glucose deprivation/reoxygenation (OGD/R)-stimulated TCMK-1 cells by lactate dehydrogenase (LDH) release assay, CCK-8 assay,enzyme-linked immunosorbent assay (ELISA), flow cytometric analysis, immunofluorescence staining,RT-qPCRand western blot analysis in vitro. We found that the levels of Tisp40 and GSDMD-N expression increased gradually, and peaked at 30 min ischemia/24 h reperfusion in vivo and 24 h OGD/R/6 h reoxygenation in vitro, simultaneously, the levels of TEC pyroptosis and renal injury were correspondingly increased. The data of Pearson's correlation analysis showed that the expression of Tisp40 and GSDMD-N was positively correlated. Furthermore, Tisp40 overexpression aggravated TEC pyroptosis rate and increased the expressions of related proteins, including GSDMD-N, NLRP3, caspase-1, IL-1ß, and IL-18 in the OGD/R-stimulated TCMK-1 cell line, whereas the opposite occurred in cells treated with small interfeing RNA (siRNA) targeting Tisp40. Tisp40-deficient mice showed attenuated renal IRI and pyroptosis compared with wild-type mice. In addition, Tisp40 knockout remarkably decreased the levels of GSDMD-N, IL-1ß, IL-18, NLRP3, and caspase-1 expression, and alleviated renal pyroptosis induced by I/R. Importantly, Tisp40 overexpression significantly increased TECs pyroptosis via p-p65 activation, however, the effects of Tisp40 overexpression were partially blocked by parthenolide (PTL). Collectively, our findings provide insight into the mechanism of how Tisp40 regulated GSDMD-mediated pyroptosis in renal IRI.

Identification of MicroRNA-92a-3p as an Essential Regulator of Tubular Epithelial Cell Pyroptosis by Targeting Nrf1 via HO-1.

Renal ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury (AKI) and has no effective treatment. Exploring the molecular mechanisms of renal IRI is critical for the prevention of AKI and its evolution to chronic kidney disease and end-stage renal disease. The aim of the present study was to determine the biological function and molecular mechanism of action of miR-92a-3p in tubular epithelial cell (TEC) pyroptosis. We investigated the relationship between nuclear factor-erythroid 2-related factor 1 (Nrf1) and TEC pyroptosis induced by ischemia-reperfusion in vivo and oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro. MicroRNAs (miRNAs) are regulators of gene expression and play a role in the progression of renal IRI. Nrf1 was confirmed as a potential target for miRNA miR-92a-3p. In addition, the inhibition of miR-92a-3p alleviated oxidative stress in vitro and decreased the expression levels of NLRP3, caspase-1, GSDMD-N, IL-1ß, and IL-18 in vitro and in vivo. Moreover, Zn-protoporphyrin-IX, an inhibitor of heme oxygenase-1, reduced the protective effect of Nrf1 overexpression on OGD/R-induced TEC oxidative stress and pyroptosis. The results of this study suggest that the inhibition of miR-92a-3p can alleviate TEC oxidative stress and pyroptosis by targeting Nrf1 in renal IRI.

Ferroelectric control of single-molecule magnetism in 2D limit.

The electric control of magnetic properties based on magnetoelectric effect is crucial for the development of future data storage devices. Here, based on first-principles calculations, a strong magnetoelectric effect is proposed to effectively switch on/off the magnetic states as well as alter the in-plane/perpendicular easy axes of metal-phthalocyanine molecules (MPc) by reversing the electric polarization of the underlying two-dimensional (2D) ferroelectric α-In2Se3 substrate with the application of an external electric field. The mechanism originates from the different hybridization between the molecule and the ferroelectric substrate in which the different electronic states of surface Se layer play a dominant role. Moreover, the magnetic moments and magnetic anisotropy energies (MAE) of OsPc/In2Se3 can be further largely enhanced by a functionalized atom atop the OsPc molecule. The I-OsPc/In2Se3 system possesses large MAE up to 30 meV at both polarization directions, which is sufficient for room-temperature applications. These findings provide a feasible scheme to realize ferroelectric control of magnetic states in 2D limit, which have great potential for applications in nanoscale electronics and spintronics.

Hydrogen sulfide treatment protects against renal ischemia-reperfusion injury via induction of heat shock proteins in rats.

OBJECTIVES: Hydrogen sulfide (H2S) attenuates ischemia-reperfusion injury (IRI) in different organs. However, its mechanism of action in renal IRI remains unclear. The present study investigated the hypothesis that H2S attenuates renal IRI via the induction of heat shock proteins (HSPs). MATERIALS AND METHODS: Adult Wistar rats were subjected to unilateral renal ischemia for 45 min followed by reperfusion for 6 hr. One group of rats underwent I/R without treatment, one group was administered 150 µmol/l sodium hydrosulfide (NaHS) prior to I/R, one group was injected with 100 mg/kg quercetin (an HSP inhibitor) intraperitoneally prior to I/R, and another group received quercetin prior to I/R and treatment with NaHS following I/R. Two other groups underwent a sham operation and one of them received 150 µmol/l NaHS following the sham operation whereas the other received no treatment. Renal function and histological changes were compared and relevant indices of oxidative stress, apoptosis, and inflammation were examined. RESULTS: IRI increased serum creatinine and blood urea nitrogen concentrations, promoted lipid peroxidation by elevating malondialdehyde levels, suppressed superoxide dismutase activity, stimulated inflammation by inducing NF-kB, IL-2, and TLR-4 expression, and increased renal apoptosis. Levels of HSP 70, heme-oxygenase-1 (HO-1) and HSP 27 were increased following IRI and reversed following H2S treatment. H2S attenuated changes observed in pathology, lipid peroxidation, inflammation, and apoptosis following IRI. The administration of quercetin reversed all protective effects of H2S. CONCLUSION: The present study indicated that H2S protected renal tissue against IRI induced lipid peroxidation, inflammation, and apoptosis, which may be attributed to the upregulation of HSP 70, HO-1, and HSP 27.

Room-temperature ferroelectricity in MoTe2 down to the atomic monolayer limit.

Ferroelectrics allow for a wide range of intriguing applications. However, maintaining ferroelectricity has been hampered by intrinsic depolarization effects. Here, by combining first-principles calculations and experimental studies, we report on the discovery of robust room-temperature out-of-plane ferroelectricity which is realized in the thinnest monolayer MoTe2 with unexploited distorted 1T (d1T) phase. The origin of the ferroelectricity in d1T-MoTe2 results from the spontaneous symmetry breaking due to the relative atomic displacements of Mo atoms and Te atoms. Furthermore, a large ON/OFF resistance ratio is achieved in ferroelectric devices composed of MoTe2-based van der Waals heterostructure. Our work demonstrates that ferroelectricity can exist in two-dimensional layered material down to the atomic monolayer limit, which can result in new functionalities and achieve unexpected applications in atomic-scale electronic devices.

Enhanced photoelectrical response of thermodynamically epitaxial organic crystals at the two-dimensional limit.

Owing to strong light-matter interaction, two-dimensional (2D) organic crystal is regarded as promising materials for ultrasensitive photodetectors, however it still received limited success due to degraded photoelectrical response and problems in controllable growth. Here, we find the growth of 2D organic crystal obeys Gibbs-Curie-Wulff law, and develop a seed-epitaxial drop-casting method to grow millimeter-sized 1,4-bis(4-methylstyryl)benzene 2D crystals on SiO2/Si in a thermodynamically controlled process. On SiO2/Si, a distinct 2D limit effect is observed, which remarkably enhances internal photoresponsivity compared with bulk crystals. Experiment and calculation show the molecules stack more compactly at the 2D limit, thus better molecular orbital overlap and corresponding changes in the band structure lead to efficient separation and transfer of photo-generated carriers as well as enhanced photo-gating modulation. This work provides a general insight into the growth and the dimension effect of the 2D organic crystal, which is valuable for the application in high-performance photoelectrical devices.

Electronic structures of ultra-thin tellurium nanoribbons.

The structural stability and electronic properties of monolayer and bilayer tellurium nanoribbons (TNRs) with different edge structures have been systematically investigated by means of first-principles calculations, revealing that the stability of both monolayer and bilayer TNRs largely rely on their width. Regardless of width, tip TNRs are metallic, while notch TNRs are p-type-like conductors. Interestingly, both mono- and bi-layer chain TNRs exhibit a semiconductor-to-metal transition as the width increases. The electronic structures of tip and notch TNRs are mainly determined by atomic reconstruction and the unsaturated electronic states on the edges. For chain TNRs, the origin of the semiconductor-to-metal transition can be attributed to the spontaneous in-plane electronic polarization across the ribbon. Our work reveals diverse electronic properties of one-dimensional elemental tellurium nanostructures, which considerably extend the potential applications of tellurene-based materials in nanodevices.