Influence of Ferromagnetic Interlayer Exchange Coupling on Current-induced Magnetization Switching and Dzyaloshinskii-Moriya Interaction in Co/Pt/Co Multilayer System

This paper investigates the relationship among interlayer exchange coupling (IEC), Dzyaloshinskii-Moriya interaction (DMI), and multilevel magnetization switching within a Co/Pt/Co heterostructure, where varying Pt thicknesses enable control over the coupling strength. Employing Brillouin Light Scattering to quantify the effective DMI, we explore its potential role in magnetization dynamics and multilevel magnetization switching. Experimental findings show four distinct resistance states under an external magnetic field and spin Hall effect related spin current. We explain this phenomenon based on the asymmetry between Pt/Co and Co/Pt interfaces and the interlayer coupling, which, in turn, influences DMI and subsequently impacts the magnetization dynamics. Numerical simulations, including macrospin, 1D domain wall, and simple spin wave models, further support the experimental observations of multilevel switching and help uncover the underlying mechanisms. Our proposed explanation, supported by magnetic domain observation using polar-magnetooptical Kerr microscopy, offers insights into both the spatial distribution of magnetization and its dynamics for different IECs, thereby shedding light on its interplay with DMI, which may lead to potential applications in storage devices

Study of Spin-Orbit Interactions and Interlayer Ferromagnetic Coupling in Co/Pt/Co Trilayers in Wide Range of Heavy Metal Thickness

The spin-orbit torque, a torque induced by a charge current flowing through the heavy-metal conducting layer with strong spin-orbit interactions, provides an efficient way to control the magnetization direction in heavy-metal/ferromagnet nanostructures, required for applications in the emergent magnetic technologies like random access memories, high-frequency nano oscillators, or bio-inspired neuromorphic computations. We study the interface properties, magnetization dynamics, magnetostatic features and spin-orbit interactions within the multilayer system Ti(2)/Co(1)/Pt(0-4)/Co(1)/MgO(2)/Ti(2) (thicknesses in nanometers) patterned by optical lithography on micrometer-sized bars. In the investigated devices, Pt is used as a source of the spin current and as a non-magnetic spacer with variable thickness, which enables the magnitude of the interlayer ferromagnetic exchange coupling to be effectively tuned. We also find the Pt thickness-dependent changes in magnetic anisotropies, magnetoresistance, effective Hall angle and, eventually, spin-orbit torque fields at interfaces. The experimental findings are supported by the relevant interface structure-related simulations, micromagnetic, macrospin, as well as the spin drift-diffusion models. Finally, the contribution of the spin-orbital Edelstein-Rashba interfacial fields is also briefly discussed in the analysis.Comment: 39 pages, 14 figure

Heme oxygenase-1 is required for angiogenic function of bone marrow-derived progenitor cells : role in therapeutic revascularization

Aims: Heme oxygenase-1 (HO-1) is a cytoprotective enzyme that can be down-regulated in diabetes. Its importance for mature endothelium has been described, but its role in proangiogenic progenitors is not well known. We investigated the effect of HO-1 on the angiogenic potential of bone marrow-derived cells (BMDCs) and on blood flow recovery in ischemic muscle of diabetic mice. Results: Lack of HO-1 decreased the number of endothelial progenitor cells (Lin−CD45−cKit-Sca-1+VEGFR-2+) in murine bone marrow, and inhibited the angiogenic potential of cultured BMDCs, affecting their survival under oxidative stress, proliferation, migration, formation of capillaries, and paracrine proangiogenic potential. Transcriptome analysis of HO-1−/− BMDCs revealed the attenuated up-regulation of proangiogenic genes in response to hypoxia. Heterozygous HO-1+/− diabetic mice subjected to hind limb ischemia exhibited reduced local expression of vascular endothelial growth factor (VEGF), placental growth factor (PlGF), stromal cell-derived factor 1 (SDF-1), VEGFR-1, VEGFR-2, and CXCR-4. This was accompanied by impaired revascularization of ischemic muscle, despite a strong mobilization of bone marrow-derived proangiogenic progenitors (Sca-1+CXCR-4+) into peripheral blood. Blood flow recovery could be rescued by local injections of conditioned media harvested from BMDCs, but not by an injection of cultured BMDCs. Innovation: This is the first report showing that HO-1 haploinsufficiency impairs tissue revascularization in diabetes and that proangiogenic in situ response, not progenitor cell mobilization, is important for blood flow recovery. Conclusions: HO-1 is necessary for a proper proangiogenic function of BMDCs. A low level of HO-1 in hyperglycemic mice decreases restoration of perfusion in ischemic muscle, which can be rescued by a local injection of conditioned media from cultured BMDCs

Heme Oxygenase-1 Accelerates Cutaneous Wound Healing in Mice

Heme oxygenase-1 (HO-1), a cytoprotective, pro-angiogenic and anti-inflammatory enzyme, is strongly induced in injured tissues. Our aim was to clarify its role in cutaneous wound healing. In wild type mice, maximal expression of HO-1 in the skin was observed on the 2nd and 3rd days after wounding. Inhibition of HO-1 by tin protoporphyrin-IX resulted in retardation of wound closure. Healing was also delayed in HO-1 deficient mice, where lack of HO-1 could lead to complete suppression of reepithelialization and to formation of extensive skin lesions, accompanied by impaired neovascularization. Experiments performed in transgenic mice bearing HO-1 under control of keratin 14 promoter showed that increased level of HO-1 in keratinocytes is enough to improve the neovascularization and hasten the closure of wounds. Importantly, induction of HO-1 in wounded skin was relatively weak and delayed in diabetic (db/db) mice, in which also angiogenesis and wound closure were impaired. In such animals local delivery of HO-1 transgene using adenoviral vectors accelerated the wound healing and increased the vascularization. In summary, induction of HO-1 is necessary for efficient wound closure and neovascularization. Impaired wound healing in diabetic mice may be associated with delayed HO-1 upregulation and can be improved by HO-1 gene transfer