Spin-torque-driven antiferromagnetic resonance.

The intrinsic fast dynamics make antiferromagnetic spintronics a promising avenue for faster data processing. Ultrafast antiferromagnetic resonance-generated spin current provides valuable access to antiferromagnetic spin dynamics. However, the inverse effect, spin-torque-driven antiferromagnetic resonance (ST-AFMR), which is attractive for practical utilization of fast devices but seriously impeded by difficulties in controlling and detecting Néel vectors, remains elusive. We observe ST-AFMR in Y3Fe5O12/α-Fe2O3/Pt at room temperature. The Néel vector oscillates and contributes to voltage signal owing to antiferromagnetic negative spin Hall magnetoresistance-induced spin rectification effect, which has the opposite sign to ferromagnets. The Néel vector in antiferromagnetic α-Fe2O3 is strongly coupled to the magnetization in Y3Fe5O12 buffer, resulting in the convenient control of Néel vectors. ST-AFMR experiment is bolstered by micromagnetic simulations, where both the Néel vector and the canted moment of α-Fe2O3 are in elliptic resonance. These findings shed light on the spin current-induced dynamics in antiferromagnets and represent a step toward electrically controlled antiferromagnetic terahertz emitters.

Ultrasmall and tunable TeraHertz surface plasmon cavities at the ultimate plasmonic limit.

The ability to confine THz photons inside deep-subwavelength cavities promises a transformative impact for THz light engineering with metamaterials and for realizing ultrastrong light-matter coupling at the single emitter level. To that end, the most successful approach taken so far has relied on cavity architectures based on metals, for their ability to constrain the spread of electromagnetic fields and tailor geometrically their resonant behavior. Here, we experimentally demonstrate a comparatively high level of confinement by exploiting a plasmonic mechanism based on localized THz surface plasmon modes in bulk semiconductors. We achieve plasmonic confinement at around 1 THz into record breaking small footprint THz cavities exhibiting mode volumes as low as [Formula: see text], excellent coupling efficiencies and a large frequency tunability with temperature. Notably, we find that plasmonic-based THz cavities can operate until the emergence of electromagnetic nonlocality and Landau damping, which together constitute a fundamental limit to plasmonic confinement. This work discloses nonlocal plasmonic phenomena at unprecedentedly low frequencies and large spatial scales and opens the door to novel types of ultrastrong light-matter interaction experiments thanks to the plasmonic tunability.

Van der Waals lattice-induced colossal magnetoresistance in Cr2Ge2Te6 thin flakes.

Recent discovery of two-dimensional (2D) magnets with van der Waals (vdW) gapped layered structure prospers the fundamental research of magnetism and advances the miniaturization of spintronics. Due to their unique lattice anisotropy, their band structure has the potential to be dramatically modulated by the spin configuration even in thin flakes, which is still unexplored. Here, we demonstrate the vdW lattice-induced spin modulation of band structure in thin flakes of vdW semiconductor Cr2Ge2Te6 (CGT) through the measurement of magnetoresistance (MR). The significant anisotropic lattice constructed by the interlayer vdW force and intralayer covalent bond induces anisotropic spin-orbit field, resulting in the spin orientation-dependent band splitting. Consequently, giant variation of resistance is induced between the magnetization aligned along in-plane and out-of-plane directions. Based on this, a colossal MR beyond 1000% was realized in lateral nonlocal devices with CGT acting as a magneto switch. Our finding provides a unique feature for the vdW magnets and would advance its applications in spintronics.

Antiferromagnetic Inverse Spin Hall Effect.

The inverse spin Hall effect (ISHE) is one of the accessible and reliable methods to detect spin current. The magnetization-dependent inverse spin Hall effect has been observed in magnets, expanding the dimension for spin-to-charge conversion. However, antiferromagnetic Néel-vector-dependent ISHE, which has been long time highly pursued, is still elusive. Here, ISHE in Mn2 Au/[Co/Pd] heterostructures is investigated by terahertz emission and spin Seebeck effect measurements, where [Co/Pd] possesses perpendicular magnetic anisotropy for out-of-plane polarized spin current generation and Mn2 Au is a collinear antiferromagnet for the spin-to-charge conversion. The out-of-plane spin polarization (σz ) is rotated toward in-plane by the Néel vectors in Mn2 Au, then the spin current is converted into charge current at two staggered spin sublattices. The ISHE signal is much stronger when the converted charge current is parallel to the Néel vector compared with its orthogonal counterpart. The Néel vector and resultant ISHE signals, which is termed as antiferromagnetic inverse spin Hall effect, can be switched. The finding not only adds a new member to the Hall effect family, but also makes antiferromagnetic spintronics more flexible.

Orthogonal interlayer coupling in an all-antiferromagnetic junction.

In conventional ferromagnet/spacer/ferromagnet sandwiches, noncollinear couplings are commonly absent because of the low coupling energy and strong magnetization. For antiferromagnets (AFM), the small net moment can embody a low coupling energy as a sizable coupling field, however, such AFM sandwich structures have been scarcely explored. Here we demonstrate orthogonal interlayer coupling at room temperature in an all-antiferromagnetic junction Fe2O3/Cr2O3/Fe2O3, where the Néel vectors in the top and bottom Fe2O3 layers are strongly orthogonally coupled and the coupling strength is significantly affected by the thickness of the antiferromagnetic Cr2O3 spacer. From the energy and symmetry analysis, the direct coupling via uniform magnetic ordering in Cr2O3 spacer in our junction is excluded. The coupling is proposed to be mediated by the non-uniform domain wall state in the spacer. The strong long-range coupling in an antiferromagnetic junction provides an unexplored approach for designing antiferromagnetic structures and makes it a promising building block for antiferromagnetic devices.

Piezoelectric Strain-Controlled Magnon Spin Current Transport in an Antiferromagnet.

As the core of spintronics, the transport of spin aims at a low-dissipation data process. The pure spin current transmission carried by magnons in antiferromagnetic insulators is natively endowed with superiority such as long-distance propagation and ultrafast speed. However, the traditional control of magnon transport in an antiferromagnet via a magnetic field or temperature variation adds critical inconvenience to practical applications. Controlling magnon transport by electric methods is a promising way to overcome such embarrassment and to promote the development of energy-efficient antiferromagnetic logic. Here, the experimental realization of an electric field-induced piezoelectric strain-controlled magnon spin current transmission through the antiferromagnetic insulator in the Y3Fe5O12/Cr2O3/Pt trilayer is reported. An efficient and nonvolatile manipulation of magnon propagation/blocking is achieved by changing the relative direction between the Néel vector and spin polarization, which is tuned by ferroelastic strain from the piezoelectric substrate. The piezoelectric strain-controlled antiferromagnetic magnon transport opens an avenue for the exploitation of antiferromagnet-based spin/magnon transistors with ultrahigh energy efficiency.

Investigation of Temperature-Dependent Magnetic Properties and Coefficient of Thermal Expansion in Invar Alloys.

Invar Fe-Ni alloy is a prominent Ni steel alloy with a low coefficient of thermal expansion around room temperature. We investigate the correlation between magnetic properties and thermal expansion in cold-drawn Fe-36Ni wires with different heat treatment conditions, where the annealing parameters with furnace cooling (cooling from the annealing temperature of 300, 400, 500, 600, 700, 800, 900, and 1000 °C) are used. The variation trend of magnetic properties is consistent with that of thermal expansion for all samples, where the maximum appears at 600 °C -treated sample and 400 °C shows the minimum. The domain size and the area of domain walls determine the total energy of the domain wall, and the total energy directly determines the size of magnetostriction, which is closely related to the coefficient of thermal expansion. Also, the differential thermal analysis (DTA) shows endothermic and exothermic reactions represent crystalline transitions, which could possibly cause the abrupt change of magnetic properties and thermal expansion coefficient of materials. The results indicate that there is a certain relation between thermal expansion and magnetic properties. Besides the fundamental significance, our work provides an Invar alloy with a low coefficient of thermal expansion for practical use.

Crosstalk between DNA methylation and histone acetylation triggers GDNF high transcription in glioblastoma cells.

BACKGROUND: Glial cell line-derived neurotrophic factor (GDNF) is highly expressed in glioblastoma (GBM) and blocking its expression can inhibit the initiation and development of GBM. GDNF is a dual promoter gene, and the promoter II with two enhancers and two silencers plays a major role in transcription initiation. We had previously reported that histone hyperacetylation and DNA hypermethylation in GDNF promoter II region result in high transcription of GDNF in GBM cells, but the mechanism remains unclear. In this study, we investigated whether these modifications synergistically regulate high GDNF transcription in GBM. RESULTS: Cyclic AMP response element binding protein (CREB) expression and phosphorylation at S133 were significantly increased in human GBM tissues and GBM cell lines (U251 and U343). In U251 GBM cells, high expressed CREB significantly enhanced GDNF transcription and promoter II activity. CREB regulated GDNF transcription via the cyclic AMP response elements (CREs) in enhancer II and silencer II of GDNF promoter II. However, the two CREs played opposite regulatory roles. Interestingly, hypermethylation of CRE in silencer II occurred in GBM tissues and cells which led to decreased and increased phosphorylated CREB (pCREB) binding to silencer II and enhancer II, respectively. Moreover, pCREB recruited CREB binding protein (CBP) with histone acetylase activity to the CRE of GDNF enhancer II, thereby increasing histone H3 acetylation and RNA polymerase II recruitment there and at the transcription start site (TSS), and promoted GDNF high transcription in U251 cells. The results indicated that high GDNF transcription was attributable to DNA hypermethylation in CRE of GDNF silencer II increasing pCREB binding to CRE in enhancer II, which enhanced CBP recruitment, histone H3 acetylation, and RNA polymerase II recruitment there and at the TSS. CONCLUSIONS: Our results demonstrate that pCREB-induced crosstalk between DNA methylation and histone acetylation at the GDNF promoter II enhanced GDNF high transcription, providing a new perspective for GBM treatment.

High Concentration of Glial Cell Line-Derived Neurotrophic Factor Protects Primary Astrocytes from Apoptosis.

BACKGROUND: Studies have shown that astrocytes play an important role in a variety of biological processes, so damage to astrocytes can cause a series of related diseases. Glial cell line-derived neurotrophic factor (GDNF) has always been considered a protective factor for dopamine neurons. However, it remains unclear whether GDNF has a protective effect on glial cells, especially astrocytes. In this study, we put forward the hypothesis that a high concentration of GDNF in the microenvironment of astrocytes exerts an inhibitory effect on the apoptosis of astrocytes by DNA-damaging reagents. METHODS: We isolated, purified, and identified primary astrocytes from neonate rats. Astrocytes were exposed to mitoxantrone (MTN, a DNA-damaging compound) for 24 h. The effects of MTN on astrocytes were tested by Hoechst 33342 staining, CCK-8 assay, and flow cytometry assay. One of the concentrations of MTN was applied to construct an apoptotic model of astrocytes. The astrocytes were then treated with GDNF together with a selected concentration of MTN for 24 h. The cell viability, cell nucleus morphology, and apoptosis ratio of the cells was assessed by Hoechst 33342 staining, CCK-8 assay, and flow cytometry assay, respectively. RNA sequencing (RNA-Seq), quantitative PCR analysis, and KEGG pathway mapping were performed to examine the genes involved in the procedure. Finally, Western blot analysis was applied to confirm the expression levels of the proteins of interest. RESULTS: Hoechst 33342 staining revealed a one-tenth change in the percentage of Hoechst-positive cells after the addition of 500 ng/mL GDNF combined with 1,000 nM MTN for 24 h. The viability of the cells treated the same as described above was 1.4-fold that of the control group. Flow cytometry assays indicated that the apoptotic rates were 17.67, 8.67, and 4.34% for 0, 200, and 500 ng/mL GDNF, respectively. Birc2, Birc3, and Gadd45b were linked to the antiapoptotic process induced by GDNF in astrocytes. Western blot analysis confirmed the elevated expression of Birc2 and Gadd45b. CONCLUSIONS: Our studies revealed that GDNF has a noticeable antiapoptotic effect on gene-injured astrocytes. This may provide critical clues for the treatment of a series of diseases in which damaged astrocytes are involved.

MiRNAs Mediate GDNF-Induced Proliferation and Migration of Glioma Cells.

BACKGROUND/AIMS: Glial cell line-derived neurotrophic factor (GDNF) is an important factor promoting invasive glioma growth. This study was performed to reveal a unique mechanism of glioma cell proliferation and migration. METHODS: Human U251 glioma cells were used to screen the optimal GDNF concentration and treatment time to stimulate proliferation and migration. MicroRNA (MiRNA) expression profiles were detected by microarray and confirmed by real-time polymerase chain reaction (PCR). The target genes of differentially expressed miRNAs were predicted by miRWalk, and those targeted by multiple miRNAs were screened with Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. A regulatory miRNA network was constructed using ingenuity pathway analysis (IPA). Target gene expression of differentially expressed miRNAs was examined by real-time PCR or mRNA microarray. RESULTS: The results show that 50 ng/mL GDNF for 24 h significantly promotes U251 glioma cell proliferation and migration (P < 0.05). Seven miRNAs (hsa-miR-194-5p, hsa-miR-152-3p, hsa-miR-205-5p, hsa-miR-629-5p, hsa-miR-3609, hsa-miR-183-5p, and hsa-miR-487b-3p) were significantly up-regulated after GDNF treatment (P < 0.05). These miRNAs are primarily involved in signal transduction, cell adhesion and cell cycle through mitogen-activated protein kinase (MAPK) signaling, focal adhesion and glioma signal pathways. Five of these miRNAs (hsa-miR-194-5p, hsa-miR-152-3p, hsa-miR-205-5p, hsa-miR-183-5p, and hsa-miR-487b-3p) co-regulate TP53 and Akt. mRNA expression levels of four genes co-targeted by two or more up-regulated miRNAs were significantly decreased after GDNF treatment (P < 0.05). CONCLUSION: GDNF treatment of U251 glioma cells significantly increased the expression of seven miRNAs involved in cell adhesion and the cell cycle.

Egr-1 and RNA POL II facilitate glioma cell GDNF transcription induced by histone hyperacetylation in promoter II.

The specific mechanisms for epigenetic regulation of gene transcription remain to be elucidated. We previously demonstrated that hyperacetylation of histone H3K9 in promoter II of glioma cells promotes high transcription of the glial cell line-derived neurotrophic factor (GDNF) gene. This hyperacetylation significantly enhanced Egr-1 binding and increased the recruitment of RNA polymerase II (RNA POL II) to that region (P < 0.05). Egr-1 expression was abnormally increased in C6 glioma cells. Further overexpression of Egr-1 significantly increased Egr-1 binding to GDNF promoter II, while increasing RNA POL II recruitment, thus increasing GDNF transcription (P < 0.01). When the acetylation of H3K9 in the Egr-1 binding site was significantly reduced by the histone acetyltransferase (HAT) inhibitor curcumin, binding of Egr-1 to GDNF promoter II, RNA POL II recruitment, and GDNF mRNA expression were significantly downregulated (P < 0.01). Moreover, curcumin attenuated the effects of Egr-1 overexpression on Egr-1 binding, RNA POL II recruitment, and GDNF transcription (P < 0.01). Egr-1 and RNA POL II co-existed in the nucleus of C6 glioma cells, with overlapping regions, but they were not bound to each other. In conclusion, highly expressed Egr-1 may be involved in the recruitment of RNA POL II in GDNF promoter II in a non-binding manner, and thereby involved in regulating GDNF transcription in high-grade glioma cells. This regulation is dependent on histone hyperacetylation in GDNF promoter II.