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1.
Adv Sci (Weinh) ; 6(5): 1801663, 2019 Mar 06.
Artigo em Inglês | MEDLINE | ID: mdl-30886796

RESUMO

Water splitting is considered to be a very promising alternative to greenly produce hydrogen, and the key to optimizing this process is the development of suitable electrocatalysts. Here, a sacrificial-counter-electrode method to synthesize a MoS x /carbon nanotubes/Pt catalyst (0.55 wt% Pt loading) is developed, which exhibits a low overpotential of 25 mV at a current density of 10 mA cm-2, a low Tafel slope of 27 mV dec-1, and excellent stability under acidic conditions. The theory calculations and experimental results confirm the high hydrogen evolution activity that is likely due to the fact that the S atoms in MoS x can be substituted with O atoms during a potential cycling process when using Pt as a counter-electrode, where the O atoms act as bridges between the catalytic PtO x particles and the MoS x support to generate a MoS x -O-PtO x structure, allowing the Pt atoms to donate more electrons thus facilitating the hydrogen evolution reaction process.

2.
Cell Mol Immunol ; 2017 May 01.
Artigo em Inglês | MEDLINE | ID: mdl-28458392

RESUMO

Interleukin 17 (IL-17) is increasingly recognized as a key factor that contributes to the pathogenesis of multiple sclerosis (MS) and its experimental mouse autoimmune encephalomyelitis (EAE) model. However, the roles and regulatory mechanisms of IL-17-induced pro-inflammatory cytokine production in EAE mice remain largely unclear. In this study, the expression of IL-17, hypoxia inducible factor-1α (HIF-1α), IL-1ß, IL-6 and microRNA-497 (miR-497), as well as their intrinsic associations, was investigated using EAE model mice and cultured astrocytes exposed to IL-17 in vitro. We observed markedly increased production of IL-17, HIF-1α, IL-1ß and IL-6 in the brain tissues of EAE mice, while the expression and secretion of HIF-1α, IL-1ß and IL-6 were also significantly increased when cultured primary astrocytes from mice were stimulated with IL-17. Meanwhile, the expression of miR-497 was downregulated both in vivo and in vitro. Subsequent in vitro experiments revealed that IL-17 induced the production of IL-1ß and IL-6 in astrocytes through the upregulation of HIF-1α as a transcriptional factor, indicating that IL-17-mediated downregulation of miR-497 enhanced HIF-1α expression. Furthermore, astrocyte-specific knockdown of IL-17RA and HIF-1α or astrocyte-specific overexpression of miR-497 by infection with different lentiviral vectors containing an astrocyte-specific promotor markedly decreased IL-1ß and IL-6 production in brain tissues and alleviated the pathological changes and score of EAE mice. Collectively, these findings indicate that decreased miR-497 expression is responsible for IL-17-triggered high HIF-1α expression and consequent IL-1ß and IL-6 production by astrocytes in EAE mice.Cellular & Molecular Immunology advance online publication, 1 May 2017; doi:10.1038/cmi.2017.12.

3.
J Biol Chem ; 289(42): 28971-86, 2014 Oct 17.
Artigo em Inglês | MEDLINE | ID: mdl-25183005

RESUMO

Interleukin 17 (IL-17), produced mainly by T helper 17 (Th17) cells, is increasingly recognized as a key regulator in various autoimmune diseases, including human multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). Although several microRNAs (miRNAs) with aberrant expression have been shown to contribute to the pathogenesis of MS and EAE, the mechanisms underlying the regulation of abnormal miRNA expression in astrocytes upon IL-17 stimulation remain unclear. In the present study, we detected the changes of miRNA expression profiles both in the brain tissue of EAE mice and in cultured mouse primary astrocytes stimulated with IL-17 and identified miR-873 as one of the co-up-regulated miRNAs in vivo and in vitro. The overexpression of miR-873, demonstrated by targeting A20 (TNFα-induced protein 3, TNFAIP3), remarkably reduced the A20 level and promoted NF-κB activation in vivo and in vitro as well as increasing the production of inflammatory cytokines and chemokines (i.e. IL-6, TNF-α, MIP-2, and MCP-1/5). More importantly, silencing the endogenous miR-873 or A20 gene with lentiviral vector of miR-873 sponge (LV-miR-873 sponge) or short hairpin RNA (shRNA) of A20 (LV-A20 shRNA) in vivo significantly lessened or aggravated inflammation and demyelination in the central nervous system (CNS) of EAE mice, respectively. Taken together, these findings indicate that miR-873 induced by IL-17 stimulation promotes the production of inflammatory cytokines and aggravates the pathological process of EAE mice through the A20/NF-κB pathway, which provides a new insight into the mechanism of inflammatory damage in MS.


Assuntos
Cisteína Endopeptidases/metabolismo , Encefalomielite Autoimune Experimental/metabolismo , Interleucina-17/metabolismo , Peptídeos e Proteínas de Sinalização Intracelular/metabolismo , MicroRNAs/metabolismo , Regiões 3' não Traduzidas , Animais , Astrócitos/citologia , Astrócitos/metabolismo , Doenças Desmielinizantes , Regulação da Expressão Gênica , Inflamação , Lentivirus/genética , Camundongos , Camundongos Endogâmicos C57BL , NF-kappa B/metabolismo , Proteína 3 Induzida por Fator de Necrose Tumoral alfa
4.
J Biol Chem ; 287(20): 16410-23, 2012 May 11.
Artigo em Inglês | MEDLINE | ID: mdl-22427665

RESUMO

The apoptosis of glomerular mesangial cells (GMC) in rat Thy-1 nephritis (Thy-1N), a model of human mesangioproliferative glomerulonephritis, is accompanied by sublytic C5b-9 deposition, but the mechanism of sublytic C5b-9-mediated GMC apoptosis has not been elucidated. In the present study, the gene expression profiles both in the GMC stimulated by sublytic C5b-9 and the rat renal tissue of Thy-1N were detected using microarrays. Among the co-up-regulated genes, the up-regulation of interferon regulatory factor-1 (IRF-1) was further confirmed. Increased caspase 8 and caspase 3 expression and caspase 8 promoter activity in the GMC were also identified. Meanwhile, overexpression or knockdown of IRF-1 not only enhanced or inhibited GMC apoptosis and caspase 8 and 3 induction but also increased or decreased caspase 8 promoter activity, respectively. The element of IRF-1 binding to the caspase 8 promoter was first revealed. Furthermore, silencing IRF-1 or repressing the activation of caspases 8 and 3 significantly reduced GMC apoptosis, including other pathologic changes of Thy-1N. These novel findings indicate that GMC apoptosis of Thy-1N is associated with the IRF-1-activated caspase 8 pathway.


Assuntos
Apoptose , Caspase 8/metabolismo , Complexo de Ataque à Membrana do Sistema Complemento/metabolismo , Glomerulonefrite Membranoproliferativa/metabolismo , Fator Regulador 1 de Interferon/metabolismo , Células Mesangiais/metabolismo , Animais , Caspase 3/genética , Caspase 3/metabolismo , Caspase 8/genética , Linhagem Celular , Complexo de Ataque à Membrana do Sistema Complemento/genética , Modelos Animais de Doenças , Ativação Enzimática/efeitos dos fármacos , Ativação Enzimática/genética , Glomerulonefrite Membranoproliferativa/induzido quimicamente , Glomerulonefrite Membranoproliferativa/genética , Glomerulonefrite Membranoproliferativa/patologia , Humanos , Fator Regulador 1 de Interferon/genética , Isoanticorpos/efeitos adversos , Isoanticorpos/farmacologia , Células Mesangiais/patologia , Ratos , Elementos de Resposta/genética
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