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Articles by T Endo
Total Records ( 6 ) for T Endo
  A Miyaki , S Maeda , M Yoshizawa , M Misono , Y Saito , H Sasai , T Endo , Y Nakata , K Tanaka and R. Ajisaka
 

Obesity and reduction in central arterial distensibility, respectively, have been identified as powerful and independent risk factors for cardiovascular disease. However, the effect of weight reduction on central arterial function in obese subjects has not yet been clarified. We investigated whether low-calorie diet-induced weight reduction affects central arterial distensibility and endothelial function in middle-aged obese men. Twelve obese men (age: 45+2 yrs, BMI: 30+1 kg/m 2) completed a 12-week dietary intervention. Caloric restriction induced significantly weight loss and decrease in BMI. After the program, carotid arterial compliance significantly increased and b-stiffness index and aortic pulse-wave velocity remarkably decreased. Concentrations of plasma endothelin-1 (ET-1) significantly decreased and plasma nitric oxide (NO) markedly increased after the program. Weight reduction by low-calorie diet in obese men increases central arterial distensibility, which may contribute to the improvement in endothelial function, as noted by a decrease in ET-1 and an increase in NO.

  E Avsar Ban , H Ishikawa , H Manya , M Watanabe , S Akiyama , H Miyake , T Endo and Y. Tamaru
 

Two distinct cDNAs corresponding to two zebrafish protein O-mannosyltransferase genes, zPOMT1 and zPOMT2, were cloned from early developmental embryos. Gene expression analysis revealed that zPOMT1 and zPOMT2 were expressed in similar patterns during early embryonic development and in all adult tissues. To study the regulation of zPOMT1 and zPOMT2 mRNA distribution during zebrafish embryogenesis, we injected enhanced green fluorescent protein (EGFP) mRNA fused to the 3'untranslated regions of each zPOMT gene. The distribution of EGFP resulting from the two constructs was similar. Injection of antisense morpholino oligonucleotides of zPOMT1 and zPOMT2 resulted in several severe phenotypes—including bended body, edematous pericaridium and abnormal eye pigmentation. Immunohistochemistry using anti-glycosylated -dystroglycan antibody (IIH6) and morphological analysis revealed that the phenotypes of zPOMT2 knockdown were more severe than those of zPOMT1 knockdown, even though the IIH6 reactivity was lost in both zPOMT1 and zPOMT2 morphants. Finally, only when both zPOMT1 and zPOMT2 were expressed in human embryonic kidney 293T cells were high levels of protein O-mannosyltransferase activity detected, indicating that both zPOMT1 and zPOMT2 were required for full enzymatic activity. Moreover, either heterologous combination, zPOMT1 and human POMT2 (hPOMT2) or hPOMT1 and zPOMT2, resulted in enzymatic activity in cultured cells. These results indicate that the protein O-mannosyltransferase machinery in zebrafish and humans is conserved and suggest that zebrafish may be useful for functional studies of protein O-mannosylation.

  A Komaru , N Kamiya , H Suzuki , T Endo , M Takano , M Yano , K Kawamura , T Imamoto and T. Ichikawa
  Objective

To determine the association between obesity and prostate cancer in Japanese recurrence after primary treatment with radical prostatectomy.

Methods

The subjects were 173 Japanese patients with prostate cancer who had been treated with radical prostatectomy at Chiba University Hospital between April 1997 and March 2007. Clinicopathological characteristics and biochemical recurrence outcomes after radical prostatectomy were compared between the three body mass index cohorts.

Results

Mean body mass index was 23.4 kg/m2 with a standard deviation of 2.4, and mean follow-up period was 37.4 months. Operative time was longer and estimated blood loss was much more in obese patients. Patients with pT3≥ had significantly higher serum prostate-specific antigen, total cholesterol levels, Gleason's sum and positive of surgical margin than pT2 patients. Recurrence rate was significantly higher in the 26.5 kg/m2 and hyperlipidemia groups in pT3≥ patients.

Conclusions

Obesity is an independent predictor of disease recurrence in Japanese patients with pT3≥ prostate cancer who underwent radical prostatectomy. Obese patients who underwent radical prostatectomy require vigilant follow-up care.

  M Ruprecht , T Bionda , T Sato , M. S Sommer , T Endo and E. Schleiff
 

Protein translocation across membranes is a fundamental cellular process. The majority of the proteins of organelles such as mitochondria and chloroplasts is synthesized in the cytosol and subsequently imported in a post-translational manner. The precursor proteins have to be unfolded at least for translocation, but it has also been assumed that they are unfolded during transport to the organelle in the cytosol. Unfolding is governed by chaperones and the translocon itself. At the same time, chaperones provide the energy for the import process. The energetic properties of the chloroplast translocon were studied by import of the Ig-like module of the muscle protein titin fused to the transit peptide of the chloroplast targeted oxygen evolving complex subunit of 33 kDa (OE33). Our results suggest that p(OE33)titin is folded prior to import and that translocation is initiated by unfolding after having bound to the translocon at the chloroplast surface. Using a set of stabilizing and destabilizing mutants of titin previously analyzed by atomic force microscopy and as passenger for mitochondrial translocation, we studied the unfolding force provided by the chloroplast translocon. Based on these results, a model for translocation is discussed.

  T Endo , K Kano , R Motoki , K Hama , S Okudaira , M Ishida , H Ogiso , M Tanaka , N Matsuki , R Taguchi , M Kanai , M Shibasaki , H Arai and J. Aoki
 

Lysophosphatidic acid (LPA) is a simple phospholipid but has numerous biological effects through a series of G-protein-coupled receptors specific to LPA. In general, LPA is short-lived when applied in vivo, which hinders most pharmacological experiments. In our continuing study to identify stable LPA analogues capable of in vivo applications, we identified here lysophosphatidylmethanol (LPM) as a stable and pan-LPA receptor agonist. A synthetic LPM activated all five LPA receptors (LPA1–5), and stimulates both cell proliferation and LPA-receptor-dependent cell motility. In addition, LPM showed a hypertensive effect in rodent when applied in vivo. We found that, when fetal calf serum was incubated in the presence of methanol, formation of LPM occurred rapidly, whereas it was completely blocked by depletion of autotaxin (ATX), a plasma enzyme that converts lysophosphatidylcholine (LPC) to LPA. When recombinant ATX was incubated with LPC in the presence of methanol, both LPM and LPA were produced with a ratio of 1:10, showing that ATX has transphosphatidylation activity in addition to its lysophospholipase D activity. Administration of methanol in mice resulted in the formation of several micromoles of LPM in plasma, which is much higher than that of LPA. The present study identified LPM as a novel and stable lysophospholipid mediator with LPA-like activities and ATX as a potential synthetic enzyme for LPM.

  Y Tamura , T Endo , M Iijima and H. Sesaki
 

Cardiolipin, a unique phospholipid composed of four fatty acid chains, is located mainly in the mitochondrial inner membrane (IM). Cardiolipin is required for the integrity of several protein complexes in the IM, including the TIM23 translocase, a dynamic complex which mediates protein import into the mitochondria through interactions with the import motor presequence translocase–associated motor (PAM). In this study, we report that two homologous intermembrane space proteins, Ups1p and Ups2p, control cardiolipin metabolism and affect the assembly state of TIM23 and its association with PAM in an opposing manner. In ups1 mitochondria, cardiolipin levels were decreased, and the TIM23 translocase showed altered conformation and decreased association with PAM, leading to defects in mitochondrial protein import. Strikingly, loss of Ups2p restored normal cardiolipin levels and rescued TIM23 defects in ups1 mitochondria. Furthermore, we observed synthetic growth defects in ups mutants in combination with loss of Pam17p, which controls the integrity of PAM. Our findings provide a novel molecular mechanism for the regulation of cardiolipin metabolism.

 
 
 
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