THE TARGET GENE FOR PPARα AND PPARγ IN HUVEC

HUVEC 中 PPARα 和 PPARγ 的靶基因

• 批准号: 11671135
• 负责人: INOUE Ikuo
• 金额: $ 1.86万
• 依托单位: Saitama Medical School
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1999
• 资助国家: 日本
• 起止时间: 1999 至 2000
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11671135/
• 关键词: peroxisome proliferator-activated receptor α (PPARα); peroxisome proliferator-activated receptor γ (PPARγ); human umbilical vein endothelial cells (HUVEC); nicotine adenine dinucleotide phosphate (NADPH) oxidase; cyclooxygenase-2; interleukin-1β; Cu

We examined the effects of peroxisome proliferator-activated receptor α (PPARα) and PPARγ 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). PPARα and PPARγ significantly reduced interleukin-1β and -6 mRNA expression and their protein levels in the culture medium, and also inhibited cyclooxygenase-2 mRNA expression and their protein levels. Moreover, the mRNA levels of p22phox, a 22-kD subunit and the protein levels of p47phox, a 47-kD subunit of nicotine adenine dinucleotide phosphate (NADPH) oxidase, was decreased by induction of PPARα and PPARγ. This unique anti-inflammatory effect in addition to its hypolipidemic action, may be beneficial in preventung the vascular complications that are induced by hyperlipidemia.

我们检测了过氧化物酶体增殖物激活受体 α (PPARα) 和 PPARγ 对炎症细胞因子的产生和表达以及对培养的人脐静脉内皮细胞 (HUVEC) 中涉及前列腺素和超氧化物产生的酶表达的影响，PPARα 和 PPARγ 显着降低了白细胞介素。培养基中-1β和-6 mRNA表达及其蛋白水平，并且还抑制环氧合酶-2 mRNA表达及其蛋白水平。 PPARα 和 PPARγ 这种独特的抗炎作用可降低 p22phox（22 kD 亚基）的 mRNA 水平和 p47phox（47 kD 烟碱腺嘌呤二核苷酸磷酸 (NADPH) 氧化酶亚基）的蛋白质水平。其降血脂作用，可能有助于预防高脂血症引起的血管并发症。

项目成果

Inoue I: "Molecular biology of lipid metabolism in vascular wall."Nippon Rinsho. 59(Sup2). 580-585 (2001)

井上一世：“血管壁脂质代谢的分子生物学。”Nippon Rinsho。

Awata T, Inoue K, Kurihara S, Ohkubo T, Inoue I, et al.: "(4) Missense Variations of the Gene Responsible for Wolfram Syndrome (WFS1/wolframin) in Japanese : Possible Contribution of the Arg456His Mutation to Type 1 Diabetes as a Nonautoimmune Genetic Bas

Awata T、Inoue K、Kurihara S、Ohkubo T、Inoue I 等人：“(4) 日语中导致 Wolfram 综合征 (WFS1/wolframin) 的基因错义变异：Arg456His 突变对 1 型糖尿病的可能贡献

Matsunaga T, Nakajima T, Sonodaq M, Kawai S, Kobayashi J, Inoue I, Katayama S, et al.: "(5) Reactive oxygen species as a risk factor in verotoxin 1-exposed rats."Biochem Biophys Res Commum. 14 : 260. 813-819 (1999)

Matsunaga T、Nakajima T、Sonodaq M、Kawai S、Kobayashi J、Inoue I、Katayama S 等人：“(5) 活性氧是维罗毒素 1 暴露大鼠的危险因素。”Biochem Biophys Res Commum。

Inoue I, et al.: "The ligands/activators for peroxisome proliferator-activated receptor alpha (PPARalpha) and PPARgamma increase Cu2+, Zn2+-superoxide dismutase and decrease p22phox message expressions in primary endothelial cells."Metabolism. 50(1). 3-11

Inoue I 等人：“过氧化物酶体增殖物激活受体 α (PPARα) 和 PPARgamma 的配体/激活剂可增加原代内皮细胞中 Cu2、Zn2-超氧化物歧化酶并减少 p22phox 信息表达。”代谢。

Awata,T.Inoue,K.Inoue,I.et al.: "Missense variations of the Gene Responsible for Wolfram Syndrome(WFS1/wolframin)in Japanese: Possible Contribution of the Arg456His Mutation to Type 1 Diabetes as a Nonautoimmune Genetic Basis.612-616, 2000"Biochem Biophys

Awata，T.Inoue，K.Inoue，I.et al.：“日语中负责 Wolfram 综合征的基因 (WFS1/wolframin) 的错义变异：Arg456His 突变作为非自身免疫遗传基础对 1 型糖尿病的可能贡献。