ACS Nano
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2017
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IF 13.942
Youqian Xu,Jinbo Fei,Guangle Li,Tingting Yuan,Junbai Li
Molecule assembly and functionalization of protocells have achieved a great success. However, the yield efficiency of photophosphorylation in the present cell-like systems is limited. Herein, inspired by natural photobacteria, we construct a protocell membrane reconstituting motor protein for highly efficient light-mediated adenosine triphosphate (ATP) synthesis through a layer-by-layer technique. The assembled membrane, compartmentally integrating photoacid generator, proton conductor, and ATP synthase, possesses excellent transparency, fast proton production, and quick proton transportation. Remarkably, these favorable features permit the formation of a large proton gradient in a confined region to drive ATP synthase to produce ATP with high efficiency (873 ATP s–1). It is the highest among the existing artificial photophosphorylation systems. Such a biomimetic system provides a bioenergy-supplying scenario for early photosynthetic life and holds promise in remotely controlled ATP-consumed biosensors, biocatalysts, and biodevices.
研究领域:
生物化学
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生物物理学
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合成生物学
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仿生系统
✓ 已验证
DOI
PubMed
高影响因子
eLife
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2024
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IF 6.4
Zeina Salloum,Kristin Dauner,Yun-feng Li,Neha Verma,David Valdivieso-González,Víctor Almendro-Vedia,John D Zhang,Kiran Nakka,Mei Xi Chen,Jeffrey McDonald,Chase D Corley,Alexander Sorisky,Bao-Liang Song,Iván López-Montero,Jie Luo,Jeffrey F Dilworth,Xiaohui Zha
Statins are known to be anti-inflammatory, but the mechanism remains poorly understood. Here, we show that macrophages, either treated with statin in vitro or from statin-treated mice, have reduced cholesterol levels and higher expression of Jmjd3, a H3K27me3 demethylase. We provide evidence that lowering cholesterol levels in macrophages suppresses the adenosine triphosphate (ATP) synthase in the inner mitochondrial membrane and changes the proton gradient in the mitochondria. This activates nuclear factor kappa-B (NF-κB) and Jmjd3 expression, which removes the repressive marker H3K27me3. Accordingly, the epigenome is altered by the cholesterol reduction. When subsequently challenged by the inflammatory stimulus lipopolysaccharide (M1), macrophages, either treated with statins in vitro or isolated from statin-fed mice, express lower levels proinflammatory cytokines than controls, while augmenting anti-inflammatory Il10 expression. On the other hand, when macrophages are alternatively activated by IL-4 (M2), statins promote the expression of Arg1, Ym1, and Mrc1. The enhanced expression is correlated with the statin-induced removal of H3K27me3 from these genes prior to activation. In addition, Jmjd3 and its demethylase activity are necessary for cholesterol to modulate both M1 and M2 activation. We conclude that upregulation of Jmjd3 is a key event for the anti-inflammatory function of statins on macrophages.
研究领域:
免疫学
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药理学
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细胞生物学
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表观遗传学
✓ 已验证
DOI
PubMed
高影响因子
Journal of Functional Foods
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2019
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IF 3.197
Zhenlong Chen,Yuhui Yang,Shumei Mi,Qingsheng Fan,Xiaoming Sun,Baichuan Deng,Guoyao Wu,Yafei Li,Quancheng Zhou,Zheng Ruan
Chlorogenic acid (CGA) is a type of phenolic acid that has antioxidant and anti-inflammatory activities. In this study, we investigated the hepatoprotective effect of CGA in lipopolysaccharide (LPS)-treated rats. Supplementation with CGA attenuated ( P < 0.05) hepatocyte necrosis and inflammatory cell infiltration, decreased ( P < 0.05) the activities of serum transaminases and alkaline phosphatase and the level of total bilirubin, and increased ( P < 0.05) the level of serum total protein in comparison with the LPS-only group. In addition, CGA potently inhibited ( P < 0.05) the LPS-induced drop in the activities of mitochondrial NADH dehydrogenase and ATP synthase and the contents of ATP and AMP in the liver. Furthermore, CGA could partially counteract the changes induced by lipopolysaccharide in many metabolic pathways, such as energy metabolism, amino acid metabolism, and glutathione metabolism. In summary, our study showed that CGA supplementation had a protective effect against LPS-induced chronic liver injury.
研究领域:
药理学
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肝病学
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免疫学
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代谢学
✓ 已验证
DOI
高影响因子
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