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Articles by H. Tanaka
Total Records ( 8 ) for H. Tanaka
  N Yoshikawa , M Nagasaki , M Sano , S Tokudome , K Ueno , N Shimizu , S Imoto , S Miyano , M Suematsu , K Fukuda , C Morimoto and H. Tanaka
 

Recent studies have documented various roles of adrenal corticosteroid signaling in cardiac physiology and pathophysiology. It is known that glucocorticoids and aldosterone are able to bind glucocorticoid receptor (GR) and mineralocorticoid receptor, and these ligand-receptor interactions are redundant. It, therefore, has been impossible to delineate how these nuclear receptors couple with corticosteroid ligands and differentially regulate gene expression for operation of their distinct functions in the heart. Here, to particularly define the role of GR in cardiac muscle cells, we applied a ligand-based approach involving the GR-specific agonist cortivazol (CVZ) and the GR antagonist RU-486 and performed microarray analysis using rat neonatal cardiomyocytes. We indicated that glucocorticoids appear to be a major determinant of GR-mediated gene expression when compared with aldosterone. Moreover, expression profiles of these genes highlighted numerous roles of glucocorticoids in various aspects of cardiac physiology. At first, we identified that glucocorticoids, via GR, induce mRNA and protein expression of a transcription factor Kruppel-like factor 15 and its downstream target genes, including branched-chain aminotransferase 2, a key enzyme for amino acid catabolism in the muscle. CVZ treatment or overexpression of KLF15 decreased cellular branched-chain amino acid concentrations and introduction of small-interfering RNA against KLF15 cancelled these CVZ actions in cardiomyocytes. Second, glucocorticoid-GR signaling promoted gene expression of the enzymes involved in the prostaglandin biosynthesis, including cyclooxygenase-2 and phospholipase A2 in cardiomyocytes. Together, we may conclude that GR signaling should have distinct roles for maintenance of cardiac function, for example, in amino acid catabolism and prostaglandin biosynthesis in the heart.

  J. Toyama , H. Tanaka , A. Horie , T. Uchiyama and R. Akashi
  Thirteen Cucurbitaceae species have been investigated for anti-H activity of seed lectins. The lectin was extracted from seed powder and concentrated by ethanol precipitation method. Momordica charantia, Trichosanthes kirilowii, T. cucumeroides and T. bracteata had potent hemagglutinating (HA) activity toward human type-H(O) erythrocytes, in which M. charantia exhibited considerably lower activity toward human type-Omh (para-Bombay, H-deficient). Hence, it was characterized as anti-H activity. Eight Japanese cultivars exhibited almost same degrees of anti-H activity. A lectin from seeds of M. charantia has been purified by affinity chromatography and gel-permeation. The lectin was shown to be a glycoprotein containing approximately 10% neutral sugar, which gave a single band on native polyacrylamide gel electrophoresis (PAGE) and four bands of 31.5, 30.5, 30.0 and 28.5 kDa on SDS-PAGE under reducing conditions suggesting that the lectin is a tetramer. The HA activity was stable at 50 °C for 1 h, but sharply decreased beyond 55 °C. The lectin agglutinated human type-O erythrocytes and the agglutination was inhibited by D-galactose and its derivatives, particularly human blood type-H (O) antigen trisaccharide (Fucα1 → 2Galβ1 → 4GlcNAc). These results suggest that M. charantia seed lectin has anti-H (O) activity and D-galactose specificity. Inter-specific differences in anti-H activity of the seed among Cucurbitaceae may exist.
  H. Tanaka , J. Toyama and R. Akashi
  This study examines the function and genetic structure of Momordica charantia lectin. A galactose-binding lectin (MCL1) was purified from M. charantia seeds. The MCL1 showed highest hemagglutinating activity toward human type-O(H) erythrocytes followed by A, B and Omh (para-Bombay phenotype, also known as H-deficient secretor) erythrocytes. Moreover, we observed that MCL1 inhibited the cell-free synthesis of luciferase in a rabbit reticulocyte lysate system. The N-terminal amino acid sequence of purified MCL1 was identified and used to design degenerate oligonucleotide primers. The 3' and 5' ends of the gene coding for this protein were amplified by rapid amplification of cDNA ends, cloned and sequenced. The coding region (1641 bp, 547 amino acid residues) consisted of a 23 amino acid N-terminal signal sequence preceding an A-chain of 263 amino acid residues encoding a ribosome-inactivating protein that was joined to the B-chain of 261 amino acid residues encoding a lectin. The transcript was detected only in embryos, but hemagglutinating activity was detected both in embryos and cotyledons. These results suggest that gene expression occurred only during embryogenesis and the product accumulated in embryos and cotyledons. The MCL1 was expressed in tobacco BY-2 cells and the supernatant fluid of disrupted cells showed higher hemagglutinating activity toward human type-O(H) erythrocyte than the other tested erythrocytes. Thus, transgenic tobacco suspension culture cells harboring the cloned cDNA encoding the lectin purified from M. charantia are expected to be useful for the production of MCL1.
  J. Y Park , K Matsuo , T Suzuki , H Ito , S Hosono , T Kawase , M Watanabe , I Oze , T Hida , Y Yatabe , T Mitsudomi , T Takezaki , K Tajima and H. Tanaka
 

The main lifestyle contributor to acetaldehyde exposure is the drinking of alcoholic beverages, but tobacco smoke also makes some contribution. Although acetaldehyde is associated with upper aerodigestive tract cancer risk, in accordance with genetically determined acetaldehyde metabolism, it is unclear whether lung cancer, a representative smoking-related cancer, is associated with acetaldehyde or genes impacting its metabolism. We conducted a case–control study to examine possible interaction between smoking and aldehyde dehydrogenase 2 (ALDH2) Glu504Lys polymorphism (rs671) on the risk of lung cancer in Japanese. Subjects were 718 lung cancer cases and 1416 non-cancer controls enrolled in the Hospital-based Epidemiologic Research Program at Aichi Cancer Center. Lifestyle factors, including smoking, were determined by self-administered questionnaire. We applied pack-years (PY; categorized into five levels: never, <15, <30, <45 and ≥45) as a marker of cumulative exposure to smoking. The impact of smoking, ALDH2 genotype, and their interaction on lung cancer risk were assessed by odds ratio (OR) and 95% confidence interval adjusted for potential confounders. Adjusted ORs for PY <15, <30, <45 and ≥45 relative to never smokers among those with Glu/Glu or Glu/Lys were 1.39, 1.80, 3.44 and 6.25, respectively (P-trend = 1.4 x 10–30). In contrast, ORs among Lys/Lys were 1.01, 10.2, 11.4 and 23.2, respectively (P-trend = 2.6 x 10–7). Interaction between ALDH2 genotype (Glu/Glu + Glu/Lys versus Lys/Lys) and cumulative smoking dose was statistically significant (P = 0.036) and was consistently observed in the analysis among never-drinkers (interaction P = 0.041). These results suggest that ALDH2 Lys/Lys, a null enzyme activity genotype, modifies the impact of smoking on the risk of lung cancer.

  M. Shimabukuro , M. Higa , H. Tanaka , T. Shimabukuro , K. Yamakawa and H. Masuzaki
  Aims  Effects of pitavastatin and atorvastatin on the lipid profile and lipoprotein subclasses were compared in patients with Type 2 diabetes with dyslipidaemia.

Methods  Patients with Type 2 diabetes with hypercholesterolaemia and/or hypertriglyceridaemia were randomized to receive pitavastatin 2 mg (n = 16) or atorvastatin 10 mg (n = 15) for 6 months, and blood lipid and lipoprotein profiles and cholesterol and triglyceride contents of 20 lipoprotein subclasses, determined by high-performance liquid chromatography, were compared.

Results  At baseline, cholesterol in VLDL and LDL subclasses were increased equally in two groups of patients with diabetes as compared with normolipidaemic control subjects. As compared with baseline, serum levels of total cholesterol, LDL cholesterol, non-HDL cholesterol, LDL cholesterol:HDL cholesterol ratio and apolipoprotein B were decreased after 1, 3 and 6 months of treatment with atorvastatin and pitavastatin. Serum triglyceride levels were decreased after 1, 3 and 6 months of atorvastatin, but only at 3 months of pitavastatin. Serum HDL cholesterol was increased after 1, 3 and 6 months of pitavastatin, whereas HDL cholesterol was even decreased after 6 months of atorvastatin. Cholesterol levels of most VLDL and LDL subclasses were decreased equally in both groups. However, only pitavastatin increased cholesterol of medium HDL subclass. Serum triglyceride and triglyceride contents in VLDL and LDL subclasses were decreased only by atorvastatin.

Conclusions  The impact on lipoprotein subclass profiles was different between pitavastatin and atorvastatin. It may be beneficial to determine lipoprotein subclass profile and select the appropriate statin for each profile in patients with diabetes with an additional cardiovascular risk such as low HDL cholesterol or hypertriglyceridaemia.

 
 
 
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