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Evidence has shown that microRNAs (miRNAs/miRs) play key roles in biological functions of vascular smooth muscle cells (VSMCs). However, the role of miR-374a in VSMCs remains to be elucidated. The present study aimed to explore the influence of miR-374a on VSMCs and its molecular mechanism. The expression level of miR-374a was measured by reverse transcription-quantitative (RT-q) PCR. MTT and Transwell assay were employed to assess the role of miR-374a in proliferation and migration of VSMCs. To order to determine miR-374a targets, a dual-luciferase reporter assay was conducted, which was further verified by rescue experiments. Chromatin Immunoprecipitation Assay and JASPAR databases were applied to explore the regulatory association between GATA binding protein 2 (GATA2) and miR-374a. Western blotting or RT-qPCR were employed to detect the protein expression levels of GATA2 or RAR-related orphan receptor A (RORA). The present study found that miR-374a was elevated in VSMCs following treatment with platelet-derived growth factor-BB (PDGF-BB) compared with that in control group. In addition, the results demonstrated that a higher expression of a miR-374a could promote proliferation and migration of VSMCs while miR-374a inhibitor suppressed the PDGF-BB-induced proliferation and migration of VSMCs in vitro. Furthermore, circTADA2A bound to miR-374a and then upregulated RORA expression, which resulted in inhibition in VSMCs proliferation and migration. On the other hand, the result indicated that GATA2 overexpression could augment the proliferation, migration of PDGF-bb-induced VSMCs, which could be rescued by miR-374a inhibitor. The findings suggested that the GATA2/circTADA2A-miR-374a axis promoted the proliferation and migration of VSMCs by targeting RORA, which were closely related to atherosclerosis (AS). Thus the results might offer a new therapeutic target for AS.
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Purpose: The objective of this paper is to explore the role of circHECTD1 in vascular smooth muscle cells (VSMCs) and atherosclerosis (AS). Methods: VSMCs were treated with platelet-derived growth factor-BB (PDGF-BB) in vitro, and the level of circHECTD1 was determined using qRT-PCR. Cell proliferation, migration, and invasion were analyzed using CCK8 and transwell assays. Cell apoptosis and cell cycle were analyzed using flow cytometry. The binding interaction between circHECTD1 and KHDRBS3 or EZH2 was investigated using the RIP, RNA pull-down. Results: CircHECTD1 was upregulated in PDGF-BB-induced VSMCs with a dose-dependent and time-dependent manner. Knockdown of circHECTD1 suppressed VSMCsproliferation and migration and enhanced cell apoptosis in VSMCs, while circHECTD1 overexpression yielded opposite effects. Mechanistically, circHECTD1 could interact with KHDRBS3, thus enhanced the stability of EZH2 mRNA and increased EZH2 protein level. In addition, silencing EZH2 in VSMCs reversed the proliferation-enhancing effect of circHECTD1 overexpression. Conclusion: Our findings provided providing a potential prognostic and therapy biomarker for AS.
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Short-term plasticity (STP) is an important synaptic characteristic in the hardware implementation of artificial neural networks (ANN), as it enables the temporal information processing (TIP) capability. However, the STP feature is rather challenging to reproduce from a single nonvolatile resistive random-access memory (RRAM) element, as it requires a certain degree of volatility. In this work, a Pt/TiOx/Pt exponential selector is introduced not only to suppress the sneak current but also to enable the TIP feature in a one selector-one RRAM (1S1R) synaptic device. Our measurements reveal that the exponential selector exhibits the STP characteristic, while a Pt/HfOx/Ti RRAM enables the long-term memory capability of the synapse. Thereafter, we experimentally demonstrated pulse frequency-dependent multilevel switching in the 1S1R device, exhibiting the TIP capability of the developed 1S1R synapse. The observed STP of the selector is strongly influenced by the bottom metal-oxide interface, in which Ar plasma treatment on the bottom Pt electrode resulted in the annihilation of the STP feature in the selector. A mechanism is thus proposed to explain the observed STP, using the local electric field enhancement induced at the metal-oxide interface coupled with the drift-diffusion model of mobile O2- and Ti3+ ions. This work therefore provides a reliable means of producing the STP feature in a 1S1R device, which demonstrates the TIP capability sought after in hardware-based ANN.
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BACKGROUND: Studies have indicated vascular smooth muscle cells (VSMCs) played a crucial role in atherosclerosis and microRNAs (miRNAs) played key roles in biological functions of VSMCs. Whereas, the potential function and mechanism of miR-552 in VSMCs remains unclear. Our aim was to explore the role of miR-552 on VSMCs and underlying mechanism. MATERIAL/METHODS: MTT assay and transwell assay were used to measure the proliferation, invasion, and migration of human brain VSMCs (HBVSMCs) and mice VSMCs (mVSMCs), respectively. Bioinformatics tools and luciferase assay were adopted to verify the association between miR-552 and SKI. Rescue experiments were employed to assess the interaction of miR-552 and SKI in modulating biological functions in HBVSMCs and mVSMCs. The expression level of transcription factors (TFs)was measured via qRT-PCR assay. The effect of ATF4 on miR-552 and SKI expression was tested by qRT-PCR or western blot assay. Finally, chromatin immunoprecipitation (ChIP) assay and JASPAR databases were used to analyze the regulatory linkage between ATF4 and miR-552. RESULTS: We found that miR-552 was upregulated in HBVSMCs treated with PDGF-bb and miR-552 overexpression could promote proliferation, invasion, and migration of HBVSMCs and mVSMCs, whereas, miR-552 knockdown had the opposite impact. In addition, we also found that SKI was a direct target of miR-552, which reversed miR-552-mediated proliferation, invasion, and migration in HBVSMCs and mVSMCs. Furthermore, we also discovered that miR-552 overexpression promoted the effects of ATF4 elevation on proliferation, migration and invasion of HBVSMCs and mVSMCs, but, miR-552 decline had the opposite impact. CONCLUSIONS: ATF4-miR-552-SKI axis played critical roles in the proliferation and migration of HBVSMCs and mVSMCs, which were closely involved in atherosclerosis (AS). Therefore, our findings might offer a novel therapeutic target for AS.
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Fator 4 Ativador da Transcrição/metabolismo , Aterosclerose , MicroRNAs , Fator 4 Ativador da Transcrição/genética , Animais , Aterosclerose/metabolismo , Encéfalo/metabolismo , Movimento Celular , Proliferação de Células , Células Cultivadas , Humanos , Camundongos , MicroRNAs/metabolismo , Músculo Liso Vascular/metabolismo , Miócitos de Músculo Liso/metabolismoRESUMO
AIMS: This multicenter, open-label, randomized study (Registration No. ChiCTR-OCH-14004528) aimed to compare the efficacy and effects of oxcarbazepine (OXC) with levetiracetam (LEV) as monotherapies on patient quality of life and mental health for patients with newly diagnosed focal epilepsy from China. METHODS: Patients with newly diagnosed focal epilepsy who had experienced 2 or more unprovoked seizures at greater than a 24-h interval during the previous year were recruited. Participants were randomly assigned to the OXC group or LEV group. Efficacy, safety, quality of life, and mental health were evaluated over 12-week and 24-week periods. RESULTS: In total, we recruited 271 newly diagnosed patients from 23 centers. Forty-four patients were excluded before treatment for reasons. The rate of seizure freedom of OXC was significantly superior to that of LEV at 12 weeks and 24 weeks (p < 0.05). The quality of life (except for the seizure worry subsection) and anxiety scale scores also showed significant differences from before to after treatment in the OXC and LEV groups. CONCLUSIONS: OXC monotherapy may be more effective than LEV monotherapy in patients with newly diagnosed focal epilepsy. Both OXC and LEV could improve the quality of life and anxiety state in adult patients with focal epilepsy.
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Epilepsias Parciais , Qualidade de Vida , Adulto , Anticonvulsivantes/uso terapêutico , Epilepsias Parciais/tratamento farmacológico , Humanos , Levetiracetam/uso terapêutico , Oxcarbazepina/uso terapêutico , Convulsões/tratamento farmacológico , Resultado do TratamentoRESUMO
The growth of large-area epitaxial transition metal dichalgogenides (TMDCs) are of central importance for scalable integrated device applications. Different methods have been developed to achieve large-sized high quality films. However, reliable approaches for centimeter-sized or even wafer-level epitaxial growth of TMDCs are still lacking. Here we demonstrate a new method to grow inch-sized epitaxial WSe2 films on SiO2/Si substrates at a much lower temperature with high repeatability and scalability. High quality crystalline films are achieved through direct selenization of a tungsten film with platinum as the underlayer. The self-assembled PtSe2 buffer layer, formed during selenization, assists epitaxial growth of WSe2. Using fabricated WSe2 films, excellent performance memory devices are demonstrated. As a member of the TMDC family, our findings based on WSe2 may also be applied to other TMDC materials for large-scale production of high quality TMDC films for various applications.
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Modifying the surface energetics, particularly the work function of advanced materials, is of critical importance for a wide range of surface- and interface-based devices. In this work, using in situ photoelectron spectroscopy, we investigated the evolution of electronic structure at the SrTiO3 surface during the growth of ultra-thin MoO3 layers. Because of the large work function difference between SrTiO3 and MoO3, the energy band alignment on the SrTiO3 surface is significantly modified. The charge transfer and dipole formation at the SrTiO3-MoO3 interface leads to a large modulation of work function and to apparent doping in SrTiO3. The measured evolutions of electronic structure and upward band bending suggest that the growth of ultra-thin MoO3 layers is a powerful tool with which to modulate the surface energetics of SrTiO3, and this surface engineering approach could be generalized to other functional oxides.
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We report on the switching dynamics of P(VDF-TrEE) copolymer devices and the realization of additional substable ferroelectric states via modulation of the coupling between polarizations and space charges. The space-charge-limited current is revealed to be the dominant leakage mechanism in such organic ferroelectric devices, and electrostatic interactions due to space charges lead to the emergence of anomalous ferroelectric loops. The reliable control of ferroelectric switching in P(VDF-TrEE) copolymers opens doors toward engineering advanced organic memories with tailored switching characteristics.
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Organometal halide perovskites have recently attracted tremendous attention due to their potential for photovoltaic applications, and they are also considered as promising materials in light emitting and lasing devices. In this work, we investigated in detail the cryogenic steady state photoluminescence properties of a prototypical hybrid perovskite CH3NH3PbI3-xClx. The evolution of the characteristics of two excitonic peaks coincides with the structural phase transition around 160 K. Our results further revealed an exciton binding energy of 62.3 ± 8.9 meV and an optical phonon energy of 25.3 ± 5.2 meV, along with an abnormal blue-shift of the band gap in the high-temperature tetragonal phase.
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With a thin insulator sandwiched between two electrodes, the negative differential resistance (NDR) behavior has been frequently reported for its potential device applications. Here we report the experimental observation of a symmetric NDR characteristic in a resistive switching device based on TiO(2). We propose a charge storage mechanism for the NDR effect, with oxygen molecular ions working as the active source, in a thin insulating layer. Current-voltage measurements demonstrated a highly reproducible state at about 0.65 eV, and the photoelectron spectroscopy measurements showed that it complies well with the Ti3d band gap state. Our first-principle calculations confirm that charge storage and release arise from trapping and detrapping of oxygen molecular ions at the defect sites. The results and mechanism demonstrated here in a thin layer could be extended to other systems approaching molecular dimensions for device applications.