Myelin Activates FAK/Akt/NF-κB Pathways and Provokes CR3-Dependent Inflammatory Response in Murine System

Inflammatory response following central nervous system (CNS) injury contributes to progressive neuropathology and reduction in functional recovery. Axons are sensitive to mechanical injury and toxic inflammatory mediators, which may lead to demyelination. Although it is well documented that degenerated myelin triggers undesirable inflammatory responses in autoimmune diseases such as multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), there has been very little study of the direct inflammatory consequences of damaged myelin in spinal cord injury (SCI), i.e., there is no direct evidence to show that myelin debris from injured spinal cord can trigger undesirable inflammation in vitro and in vivo. Our data showed that myelin can initiate inflammatory responses in vivo, which is complement receptor 3 (CR3)-dependent via stimulating macrophages to express pro-inflammatory molecules and down-regulates expression of anti-inflammatory cytokines. Mechanism study revealed that myelin-increased cytokine expression is through activation of FAK/PI3K/Akt/NF-κB signaling pathways and CR3 contributes to myelin-induced PI3K/Akt/NF-κB activation and cytokine production. The myelin induced inflammatory response is myelin specific as sphingomyelin (the major lipid of myelin) and myelin basic protein (MBP, one of the major proteins of myelin) are not able to activate NF-κB signaling pathway. In conclusion, our results demonstrate a crucial role of myelin as an endogenous inflammatory stimulus that induces pro-inflammatory responses and suggest that blocking myelin-CR3 interaction and enhancing myelin debris clearance may be effective interventions for treating SCI

Enhancing the Spin–Orbit Coupling in Fe3O4 Epitaxial Thin Films by Interface Engineering

10.1021/acsami.6b0947884027353-2735

Synthesis and magnetic properties of Fe₃O₄/GaAs(100) structures for spintronics

EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Magnetic III–V Semiconductor-Based Hybrid Structures

Handbook of Spintronic

Enhancing the Spin–Orbit Coupling in Fe₃O₄ Epitaxial Thin Films by Interface Engineering

By analyzing the in-plane angular dependence of ferromagnetic resonance linewidth, we show that the Gilbert damping constant in ultrathin Fe₃O₄ epitaxial films on GaAs substrate can be enhanced by thickness reduction and oxygen vacancies in the interface. At the same time, the uniaxial magnetic anisotropy due to the interface effect becomes significant. Using the element-specific technique of X-ray magnetic circular dichroism, we find that the orbital-to-spin moment ratio increases with decreasing film thickness, in full agreement with the increase in the Gilbert damping obtained for these ultrathin single-crystal films. Combined with the first-principle calculations, the results suggest that the bonding with Fe and Ga or As ions and the ionic distortion near the interface, as well as the FeO defects and oxygen vacancies, may increase the spin–orbit coupling in ultrathin Fe₃O₄ epitaxial films and in turn provide an enhanced damping