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Articles by K Hashimoto
Total Records ( 5 ) for K Hashimoto
  T Satoh , T Ishizuka , T Tomaru , S Yoshino , Y Nakajima , K Hashimoto , N Shibusawa , T Monden , M Yamada and M. Mori
 

The 26S proteasome, which degrades ubiquitinated proteins, appears to contribute to the cyclical loading of androgen receptor (AR) to androgen response elements of target gene promoters; however, the mechanism whereby the 26S proteasome modulates AR recruitment remains unknown. Using yeast two-hybrid screening, we previously identified Tat-binding protein-1 (TBP-1), an adenosine triphosphatase of 19S regulatory particles of the 26S proteasome, as a transcriptional coactivator of thyroid hormone receptor. Independently, TBP-1-interacting protein (TBPIP) was also identified as a coactivator of several nuclear receptors, including AR. Here, we investigated whether TBP-1 could interact with and modulate transcriptional activation by AR cooperatively with TBPIP. TBP-1 mRNA was ubiquitously expressed in human tissues, including the testis and prostate, as well as in LNCaP cells. TBP-1 directly bound TBPIP through the amino-terminal domain possessing the leucine zipper structure. AR is physically associated with TBP-1 and TBPIP in vitro and in LNCaP cells. TBP-1 similarly and additively augmented AR-mediated transcription upon coexpression with TBPIP, and the ATPase domain, as well as leucine zipper structure in TBP-1, was essential for transcriptional enhancement. Overexpression of TBP-1 did not alter AR protein and mRNA levels. In the chromatin immunoprecipitation assay, TBP-1 was transiently recruited to the proximal androgen response element of the prostate-specific antigen gene promoter in a ligand-dependent manner in LNCaP cells. These findings suggest that a component of 19S regulatory particles directly binds AR and might participate in AR-mediated transcriptional activation in cooperation with TBPIP.

  K Hashimoto , E Ishida , S Matsumoto , S Okada , M Yamada , T Satoh , T Monden and M. Mori
 

The molecular mechanism of thyroid hormone (TH) effects to fatty acid metabolism in liver is yet to be clear. The carbohydrate response element-binding protein (ChREBP) as well as sterol response element-binding protein (SREBP)-1c plays a pivotal role in hepatic lipogenesis. Both SREBP-1c and ChREBP are target genes of liver X receptors (LXRs). Because LXRs and TH receptors (TRs) cross talk mutually in many aspects of transcription, we examined whether TRs regulate the mouse ChREBP gene expression. In the current study, we demonstrated that TH up-regulated mouse ChREBP mRNA and protein expression in liver. Run-on and luciferase assays showed that TH and TR-β1 positively regulated the ChREBP gene transcription. The mouse ChREBP gene promoter contains two direct repeat-4 sites (LXRE1 and LXRE2) and EMSAs demonstrated that LXR- and TR-β1 prefer to bind LXRE1 and LXRE2, respectively. The direct repeat-4 deletion and LXRE2 mutants of the promoter deteriorate the positive regulation by TR-β1, indicating that LXRE2 is functionally important for the regulation. We also showed that human ChREBP gene expression and promoter activities were up-regulated by TH. These data suggest that ChREBP mRNA expression is positively regulated by TR-β1 and TH at the transcriptional level in mammals. This novel observation indicates that TH fine-tunes hepatic lipogenesis via regulating SREBP-1c and ChREBP gene expression reciprocally.

  R Umezawa , M Yamada , K Horiguchi , S Ishii , K Hashimoto , S Okada , T Satoh and M. Mori
 

We reported a novel mutation of thyroid hormone receptor (TR)-β, F455S, in a patient with pituitary resistance to thyroid hormone (RTH), who showed impaired release of nuclear receptor corepressor and abnormal histone deacetylation. In the present study, we further analyzed the histone modifications and the dynamics of TR and RNA polymerase II on the TRH gene. The lysine residues 9 (H3K9) and 14 (K14) of the histone H3 were acetylated in the absence of thyroid hormone (TH), and addition of TH caused a temporary deacetylation of both residues. Although H3K4 was di- and trimethylated in the absence of T3, no methylation of H3K9 or K27 was detected. Long-term incubation with T3 decreased the level of trimethylated H3K4, the amount of TR, and the level of phosphorylated RNA polymerase II but not dimethylated H3K4. Treatment with an inhibitor for H3K4 methyltransferase, 5'-deoxy-5'-methylthioadenosine, decreased basal promoter activity but did not affect the repression by TH. Conversely, overexpression of MLL, an H3K4-specific methyltransferase, caused an increase in basal activity. In the presence of F455S, methylation of H3K4 and the dynamics of TR were intact, but both H3K9 and H3K14 were hyperacetylated, and T3-induced deacetylation was impaired, resulting in a high transcriptional level. These findings demonstrated that 1) negative regulation of the TRH gene by TH involves both the acetylation and methylation of specific residues of histone tails and changing the amount of TR, and 2) the major impairment to histone modifications in F455S was hyperacetylation of the specific histone tails.

  K Nakano , T Higashi , R Takagi , K Hashimoto , Y Tanaka and S. Matsushita
 

A major neurotransmitter dopamine transmits signals via five different seven transmembrane G protein-coupled receptors termed D1–D5. It is now evident that dopamine is released from leukocytes and acts as autocrine or paracrine immune modulator. However, the role of dopamine for dendritic cells (DCs) and Th differentiation remains unclear. We herein demonstrate that human monocyte-derived dendritic cells (Mo-DCs) stored dopamine in the secretary vesicles. The storage of dopamine in Mo-DCs was enhanced by forskolin and dopamine D2-like receptor antagonists via increasing cyclic adenosine 3',5'-monophosphate (cAMP) formation. Antigen-specific interaction with naive CD4+ T cells induced releasing dopamine-including vesicles from Mo-DCs. In naive CD4+ T cells, dopamine dose dependently increased cAMP levels via D1-like receptors and shifts T-cell differentiation to Th2, in response to anti-CD3 plus anti-CD28 mAb. Furthermore, we demonstrated that dopamine D2-like receptor antagonists, such as sulpiride and nemonapride, induced a significant DC-mediated Th2 differentiation, using mixed lymphocyte reaction between human Mo-DCs and allogeneic naive CD4+ T cells. When dopamine release from Mo-DCs is inhibited by colchicines (a microtubule depolymerizer), T-cell differentiation shifts toward Th1. These findings identify DCs as a new source of dopamine, which functions as a Th2-polarizing factor in DC-naive T-cell interface.

  K Hashimoto , S. i Hisasue , N Masumori , K Kobayashi , R Kato , F Fukuta , A Takahashi , T Hasegawa and T. Tsukamoto
  Objective

We investigated the clinical safety and feasibility of an algorithm we developed for the decision-making on neurovascular bundle preservation in radical prostatectomy to decrease the incidence of positive surgical margins.

Methods

We prospectively applied our algorithm to 82 patients (164 prostate sides) with clinically localized prostate cancer who underwent radical prostatectomy at our institution between October 2004 and September 2006. The algorithm was developed using the apical core characteristics, clinical T stage, preoperative prostate-specific antigen level and Gleason sum. All prostate sides were divided into two groups by the algorithm: 115 sides (70.1%) were qualified for neurovascular bundle preservation (favorable algorithm side group) and 49 sides (29.9%) for non-neurovascular bundle preservation (unfavorable algorithm side group).

Results

Median patient age was 66 years (range: 52–77) and median prostate-specific antigen was 7.1 ng/ml (range: 1.4–29.6). Overall, a positive surgical margin was observed in 23 sides (14.0%). The incidence of positive surgical margins at the apex was significantly correlated with the maximal diameter of the tumor in the apex (P < 0.001). The incidence of positive surgical margins was 8.7% in the favorable algorithm group, whereas it was 26.5% in the unfavorable algorithm group (P = 0.003). When this algorithm was combined with surgeons' intraoperative assessments, the incidence of positive surgical margins was 2.1% in neurovascular bundle preservation sides, compared with 25.0% in non-neurovascular bundle preservation sides (P = 0.002).

Conclusions

This simple algorithm is safe and feasible for the decision-making on neurovascular bundle preservation from the aspect of cancer control in radical prostatectomy patients.

 
 
 
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