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Shigeru Hokari

Researcher at Saitama Medical University

Publications -  58
Citations -  1990

Shigeru Hokari is an academic researcher from Saitama Medical University. The author has contributed to research in topics: Alkaline phosphatase & NADPH oxidase. The author has an hindex of 19, co-authored 58 publications receiving 1898 citations.

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Lipophilic HMG-CoA reductase inhibitor has an anti-inflammatory effect

TL;DR: In this paper, the effects of four 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (pravastatin, simvastatin and fluvastatatin) on the production and expression of inflammatory cytokines and on enzyme expression involving prostaglandin and superoxide production in cultured human umbilical vein endothelial cells (HUVEC) were examined.
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Mechanisms involved in valvuloseptal endocardial cushion formation in early cardiogenesis: Roles of transforming growth factor (TGF)‐β and bone morphogenetic protein (BMP)

TL;DR: Three‐dimensional collagen gel culture experiments of the AV endocardium show that myocardially derived inductive signals upregulate the expression of AV endothelial TGFβ3 at the onset of EMT, and TGF β3 needs to be expressed by these endothelial cells to trigger the initial phenotypic changes of E MT.
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The ligands/activators for peroxisome proliferator-activated receptor α (PPARα) and PPARγ increase Cu2+, Zn2+-superoxide dismutase and decrease p22phox message expressions in primary endothelial cells

TL;DR: The results suggest that PPARalpha and PPARgamma gene and protein expression in endothelial cells may play a physiologic role as radical scavengers, although the details of these mechanisms remain to be established.
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Alkaline phosphatases reduce toxicity of lipopolysaccharides in vivo and in vitro through dephosphorylation.

TL;DR: The results strongly suggest that the APs reduced the toxicity of LPS, as a host defense factor against LPS.
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NF-κB activation in endothelial cells treated with oxidized high-density lipoprotein

TL;DR: Taking all of the above findings together, ox-HDL activates NF-κB via binding to LOX-1 on the cell surface, followed by enhancement of intracellular ROS production in endothelial cells.