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Articles by H Okada
Total Records ( 3 ) for H Okada
  H Ootsuji , M Honda , S Kaneko , S Usui , M Okajima , H Okada , Y Sakai , T Takamura , K Horimoto and M. Takamura
 

Background— Acute coronary syndrome is sometimes accompanied by accelerated coagulability, lipid metabolism, and inflammatory responses, which are not attributable to the cardiac events alone. We hypothesized that the liver plays a pivotal role in the pathophysiology of acute coronary syndrome. We simultaneously analyzed the gene expression profiles of the liver and heart during acute myocardial ischemia in mice.

Methods and Results— –Mice were divided into 3 treatment groups: sham operation, ischemia/reperfusion, and myocardial infarction. Mice with liver ischemia/reperfusion were included as additional controls. Marked changes in hepatic gene expression were observed after 24 hours, despite the lack of histological changes in the liver. Genes related to tissue remodeling, adhesion molecules, and morphogenesis were significantly upregulated in the livers of mice with myocardial ischemia/reperfusion or infarction but not in those with liver ischemia/reperfusion. Myocardial ischemia, but not changes in the hemodynamic state, was postulated to significantly alter hepatic gene expression. Moreover, detailed analysis of the signaling pathway suggested the presence of humoral factors that intervened between the heart and liver. To address these points, we used isolated primary hepatocytes and showed that osteopontin released from the heart actually altered the signaling pathways of primary hepatocytes to those observed in the livers of mice under myocardial ischemia. Moreover, osteopontin stimulated primary hepatocytes to secrete vascular endothelial growth factor-A, which is important for tissue remodeling.

Conclusions— Hepatic gene expression is potentially regulated by cardiac humoral factors under myocardial ischemia. These results provide new insights into the pathophysiology of acute coronary syndrome.

  M Yamaguchi , H Okada and Y. Namiki
 

A smart and efficient method for freeze substitution and serial sectioning of yeast cells is described. Yeast cells were placed in a single layer between two copper disks, rapidly frozen, freeze substituted and embedded in an epoxy resin. The cell layer was re-embedded by the same resin, the surface trimmed leaving 1 µm above the cell layer, and serially sectioned. The sections were collected on the two-slit grids and placed on a Formvar film mounted to cover the holes of an aluminum supporting rack. The grids were removed from the rack, stained together using a silicon tube and observed in a transmission electron microscope. The images of yeast cells observed were clear and natural, and would be useful for a detailed 3D structural analysis such as structome.

  X Liu , A Matsushima , H Okada and Y. Shimohigashi
 

Bisphenol A (BPA) strongly binds to human estrogen-related receptor (ERR). BPA is an oestrogenic endocrine disruptor that influences various physiological functions at very low doses. BPA functions as an inverse-type antagonist of ERR to retain its high basal constitutive activity by inhibiting the deactivating inverse agonist activity of 4-hydroxytamoxifen (4-OHT). We recently demonstrated that ERR receptor residues Glu275 and Arg316 function as the intrinsic binding site of BPA’s phenol-hydroxyl group. We also determined the chief importance of phenol-hydroxylArg316 hydrogen bonding and the corroborative role of phenol-hydroxylGlu275 hydrogen bonding. However, there appeared to be a distinct difference between the receptor binding modes of BPA and 4-OHT. In the present study, using tritium-labelled or non-labelled BPA and 4-OHT, we evaluated in detail the receptor binding capabilities of wild-type ERR and its mutants with amino acid alterations at positions 275 and 316. Both compounds exhibited a strong binding ability to wild-type ERR due to the hydrogen bonding to Glu275 and Arg316. However, 4-OHT revealed significantly reduced occupancy for both wild-type and mutant receptors. The data obtained suggest that 4-OHT barely binds to ERR due to the strong ability of Glu275 and Arg316 to recruit phenol compounds.

 
 
 
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