Inspired by the successful synthesis of hHv-graphane[Nano letters 15 903 (2015)], a new 2D Janus material Cu-graphane is proposed based on the first-principle calculations. Without spin-orbit coupling (SOC) effect, Cu-graphane is a Dirac semimetal with a highly anisotropic Dirac cone, whose Fermi velocity ranges from 0.18×105 to 2.9×105 m/s. The Dirac cone near the Fermi level can be well described with an extended 2D Dirac model Hamiltonian. In the presence of SOC effect, band splitting is observed around the Fermi level, and a large intrinsic spin Hall conductivity with a maximum value of 346 (□/e)·S/cm is predicted. Moreover, the spin Hall transport can be regulated by slightly adjusting the Fermi energy, e.g., grid voltage or chemical doping. Our work not only proposes a new 2D Janus material with a highly anisotropic Dirac cone and a large intrinsic spin Hall conductivity, but also reveals that a large spin Hall conductivity may exist in some Dirac systems.
Background
Cardiac apoptosis plays an important role in the development of heart failure, and Angiotensin II (Ang II) plays a central role in the pathogenesis of RAAS-triggered cardiac apoptosis. Interleukin (IL)-22 is an inflammatory cytokine, which is involved in cardiovascular diseases. Recent evidence has demonstrated that there is a close relationship between IL-22 and human hypertension. However, the effects of IL-22 on Ang II-induced cardiomyocyte apoptosis remain unknown.
Methods
MCM cells and primary cardiomyocytes were exposed to Ang II with or without IL-22. The activation of the apoptosis signaling pathways, reactive oxygen species (ROS), supernatant TNF-α, Fas/FsaL, mitochondrial membrane potential (MMP), cytochrome c (Cyc) and the activity of superoxide diamutase (SOD) were detected.
Results
In MCM cells and primary cardiomyocytes, flow cytometry revealed that IL-22 significantly alleviated Ang II-induced apoptosis, and IL-22 receptors (IL-22R1 and IL-10R1) levels were obviously increased. Western blotting revealed that increased cleaved Caspase 3/8 and Bax protein levels were clearly reduced after IL-22 treatment. The Fas/FsaL and TNF-α levels were identical in the cells with or without IL-22 treatment. But ROS levels were markedly reduced after IL-22 treatment via upregulation of SOD activity, and Ang II-induced decrease of MMP was improved by IL-22, reducing the release of Cyc and the levels of cleaved Caspase 9.
Conclusions
IL-22 improved Ang II-induced cardiomyocyte apoptosis via inhibiting the intrinsic apoptosis pathway.
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