Effect of pitavastatin on transactivation of human serum paraoxonase 1 gene

Ota, Kikuko; Suehiro, Tadashi; Arii, Kaoru; Ikeda, Yukio; Kumon, Yoshitaka; Osaki, Fumiaki; Hashimoto, Kozo

doi:10.1016/j.metabol.2004.06.018

Cited by 47 publications

(42 citation statements)

References 36 publications

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“…We used an expression vector of the specificity protein 1 (Sp1) for mammalian cells, as reported previously [16]. We also constructed an expression vector of SREBB-2 and a mutated form at the positions of major p44/42 MAP-kinase specific phosphorylation sites, whose Ser-432 and Ser-455 9 were substituted with Ala (pCL-SREBP-2 S432/455A) according to previous reports [18].…”

Section: Plasmid Constructs and Transfectionmentioning

confidence: 99%

“…Huh7 cells were grown to confluence and harvested, and the nuclear fraction was isolated and extracted as described previously [16,23]. EMSA was performed as described previously [16,23].…”

Section: Preparation Of Nuclear Extracts and Electrophoretic Mobilitymentioning

confidence: 99%

“…EMSA was performed as described previously [16,23]. The synthetic sense and antisense strands of oligonucleotides (-187/-159) were 5'-GGTGGGGGCTGACCGCAAGCCGCGC-3' and 5'-GGCGCGGCTTGCGGTCAGCCCCCAC-3', respectively.…”

Section: Preparation Of Nuclear Extracts and Electrophoretic Mobilitymentioning

confidence: 99%

“…We previously reported using a reporter gene assay method showing that pitavastatin enhanced the promoter activity of the PON1 gene in HepG2 cells of a human hepatocellular carcinoma cell line and in human embryonic kidney 293 (HEK293) cells through a depletion of mevalonic acid-derived farnesyl pyrophosphate [16]. Deakin et al reported that simvastatin increased sterol regulatory element-binding protein-2 (SREBP-2) binding to PON1 DNA, and that SREBP-2 up-regulated PON1 gene promoter activity in HepG2 cells [15].…”

Section: Introductionmentioning

confidence: 99%

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Pitavastatin induces PON1 expression through p44/42 mitogen-activated protein kinase signaling cascade in Huh7 cells

et al. 2009

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Section: Plasmid Constructs and Transfectionmentioning

confidence: 99%

“…Huh7 cells were grown to confluence and harvested, and the nuclear fraction was isolated and extracted as described previously [16,23]. EMSA was performed as described previously [16,23].…”

Section: Preparation Of Nuclear Extracts and Electrophoretic Mobilitymentioning

confidence: 99%

Section: Preparation Of Nuclear Extracts and Electrophoretic Mobilitymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Pitavastatin induces PON1 expression through p44/42 mitogen-activated protein kinase signaling cascade in Huh7 cells

et al. 2009

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“…Anti-oxidant action is one of the pleiotropic effects of statins [11,12]. We and other previously reported that statins enhanced the PON1 gene promoter activity in a human hepatocellular carcinoma cell line, HepG2 cells [13], or increased the serum PON1 concentrations and activities in patients with hypercholesterolemia [14].…”

Section: Introductionmentioning

confidence: 99%

Role of protein kinase C in pitavastatin-induced human paraoxonase I expression in Huh7 cells

Arii¹,

Suehiro²,

Ikeda³

et al. 2010

Metabolism

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HDL3 stimulates paraoxonase 1 antiatherogenic catalytic and biological activities in a macrophage model system: In vivo and in vitro studies

Volkova

Aviram

2014

BioFactors

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We analyzed in-vivo and in-vitro high density lipoprotein (HDL) effects on paraoxonase 1 (PON1) antiatherogenic properties in serum and in macrophages. Intraperitoneal injection to C57BL/6 mice of recombinant PON1 (rePON1) + HDL, in comparison to HDL or to rePON1 alone, significantly increased serum PON1 arylesterase activity (by 20%), and serum-mediated cholesterol efflux from J774A.1 macrophages (by 18%). Similarly, in peritoneal macrophages (MPM) harvested from mice injected with HDL + rePON1 versus rePON1 alone, we observed reduction in oxidative stress (by 11%), increase in cellular PON1 activity (by 14%) and in HDL-mediated cholesterol efflux (by 38%). Incubation of serum or HDL with rePON1, substantially increased PON1 arylesterase activity, two-fold more than the expected additive values. HDL2 and HDL3 increased PON1 activity by 199% or 274%, respectively. Macrophage (J774A.1) cholesterol efflux rate significantly increased by HDL3 + rePON1 versus HDL3 alone (by 19%), but not by HDL2 + rePON1 versus HDL2 alone. Oxidation of HDL3 reduced its ability to induce macrophage cholesterol efflux, and abolished HDL3 stimulatory effects on rePON1. Addition of exogenous polyphenol quercetin (60 µM), but not phosphatidylcholine or apolipoprotein A1, to HDL + rePON1 increased PON1 activity (by 404%), increased the ability to reduce oxidative stress in J774A.1 macrophages (by 53%) and to stimulate macrophage cholesterol efflux (by 14%). Upon adding the hypocholesterolemic drug simvastatin (15 µg/mL) to HDL + rePON1, PON1 activity and the ability to induce macrophage cholesterol efflux increased, in comparison to HDL + rePON1. We thus concluded that HDL (mostly HDL3), stimulates PON1 antiatherogenic activities in macrophages, and these PON1 activities were further stimulated by quercetin, or by simvastatin.

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Effect of pitavastatin on transactivation of human serum paraoxonase 1 gene

Cited by 47 publications

References 36 publications

Pitavastatin induces PON1 expression through p44/42 mitogen-activated protein kinase signaling cascade in Huh7 cells

Pitavastatin induces PON1 expression through p44/42 mitogen-activated protein kinase signaling cascade in Huh7 cells

Role of protein kinase C in pitavastatin-induced human paraoxonase I expression in Huh7 cells

HDL3 stimulates paraoxonase 1 antiatherogenic catalytic and biological activities in a macrophage model system: In vivo and in vitro studies

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