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PKCη deficiency improves lipid metabolism and atherosclerosis in apolipoprotein E-deficient mice.
Torisu, Kumiko; Zhang, Xueli; Nonaka, Mari; Kaji, Takahide; Tsuchimoto, Daisuke; Kajitani, Kosuke; Sakumi, Kunihiko; Torisu, Takehiro; Chida, Kazuhiro; Sueishi, Katsuo; Kubo, Michiaki; Hata, Jun; Kitazono, Takanari; Kiyohara, Yutaka; Nakabeppu, Yusaku.
Afiliação
  • Torisu K; Division of Neurofunctional Genomics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan. torisuk@kcu.med.kyushu-u.ac.jp.
  • Zhang X; Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan. torisuk@kcu.med.kyushu-u.ac.jp.
  • Nonaka M; Division of Neurofunctional Genomics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
  • Kaji T; Division of Neurofunctional Genomics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
  • Tsuchimoto D; Translational Research Department, Sohyaku, Innovative Research Division, Mitsubishi Tanabe Pharma Corporation, 17-10 Nihonbashi, Koami-cho, Chuo-ku, Tokyo, 103-8405, Japan.
  • Kajitani K; Division of Neurofunctional Genomics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
  • Sakumi K; Research Center for Nucleotide Pool, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
  • Torisu T; Division of Neurofunctional Genomics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
  • Chida K; Counseling and Health Center, Faculty of Arts and Science, Kyushu University, 744 Motooka, Nishi-ku, Fukuoka, 819-0395, Japan.
  • Sueishi K; Division of Neurofunctional Genomics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
  • Kubo M; Research Center for Nucleotide Pool, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
  • Hata J; Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
  • Kitazono T; Department of Animal Resource Sciences, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo, 113-8657, Japan.
  • Kiyohara Y; Department of Pathology, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
  • Nakabeppu Y; Laboratory for Genotyping Development, Center for Genomic Medicine, RIKEN 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, 230-0045, Japan.
Genes Cells ; 21(10): 1030-1048, 2016 Oct.
Article em En | MEDLINE | ID: mdl-27545963
ABSTRACT
Genomewide association studies have shown that a nonsynonymous single nucleotide polymorphism in PRKCH is associated with cerebral infarction and atherosclerosis-related complications. We examined the role of PKCη in lipid metabolism and atherosclerosis using apolipoprotein E-deficient (Apoe-/- ) mice. PKCη expression was augmented in the aortas of mice with atherosclerosis and exclusively detected in MOMA2-positive macrophages within atherosclerotic lesions. Prkch+/+ Apoe-/- and Prkch-/- Apoe-/- mice were fed a high-fat diet (HFD), and the dyslipidemia observed in Prkch+/+ Apoe-/- mice was improved in Prkch-/- Apoe-/- mice, with a particular reduction in serum LDL cholesterol and phospholipids. Liver steatosis, which developed in Prkch+/+ Apoe-/- mice, was improved in Prkch-/- Apoe-/- mice, but glucose tolerance, adipose tissue and body weight, and blood pressure were unchanged. Consistent with improvements in LDL cholesterol, atherosclerotic lesions were decreased in HFD-fed Prkch-/- Apoe-/- mice. Immunoreactivity against 3-nitrotyrosine in atherosclerotic lesions was dramatically decreased in Prkch-/- Apoe-/- mice, accompanied by decreased necrosis and apoptosis in the lesions. ARG2 mRNA and protein levels were significantly increased in Prkch-/- Apoe-/- macrophages. These data show that PKCη deficiency improves dyslipidemia and reduces susceptibility to atherosclerosis in Apoe-/- mice, showing that PKCη plays a role in atherosclerosis development.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Apolipoproteínas E / Proteína Quinase C / Aterosclerose / Metabolismo dos Lipídeos Limite: Animals Idioma: En Ano de publicação: 2016 Tipo de documento: Article
Texto completo
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Apolipoproteínas E / Proteína Quinase C / Aterosclerose / Metabolismo dos Lipídeos Limite: Animals Idioma: En Ano de publicação: 2016 Tipo de documento: Article