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Articles by H Satoh
Total Records ( 4 ) for H Satoh
  H Satoh , T Moriguchi , K Taguchi , J Takai , J. M Maher , T Suzuki , P. T Winnard , V Raman , M Ebina , T Nukiwa and M. Yamamoto
 

The Nrf2 transcription factor is crucial for regulating the cellular defense against various carcinogens. However, relationship between host Nrf2 and cancer metastasis remains unexplored. To address this issue, we examined susceptibility of Nrf2-deficient mice to pulmonary cancer metastasis following implantation of the mouse Lewis lung carcinoma (3LL) cell line. Nrf2-deficient mice reproducibly exhibited a higher number of pulmonary metastatic nodules than wild-type mice did. The lung and bone marrow (BM) of cancer-bearing Nrf2-deficient mice contained increased numbers of inflammatory cells, including myeloid-derived suppressor cells (MDSCs), a potent population of immunosuppressive cells. MDSCs can attenuate CD8+ T-cell immunity through modification of the T-cell receptor complex exploiting reactive oxygen species (ROS). MDSCs of Nrf2-deficient mice retained elevated levels of ROS relative to wild-type mice. BM transplantation experiments revealed functional disturbance in the hematopoietic and immune systems of Nrf2-deficient mice. Wild-type recipient mice with Nrf2-deficient BM cells showed increased levels of lung metastasis after cancer cell inoculation. These mice exhibited high-level accumulation of ROS in MDSCs, which showed very good coincidence to the decrease of splenic CD8+ T-cells. In contrast, Keap1-knockdown mutant mice harboring high-level Nrf2 expression displayed increased resistance against the cancer cell metastasis to the lung, accompanied by a decrease in ROS in the MDSCs fraction. Our results thus reveal a novel function for Nrf2 in the prevention of cancer metastasis, presumably by its ability to preserve the redox balance in the hematopoietic and immune systems.

  M Asai , K Takeuchi , M Saotome , T Urushida , H Katoh , H Satoh , H Hayashi and H. Watanabe
  Aims

Hypoxia, ischaemia, and exogenous chemicals can induce extracellular and intracellular acidosis, but it is not clear which of these types of acidosis affects endothelial cell function. The synthesis and release of endothelium-derived relaxing factors (EDRFs) are linked to an increase in cytosolic Ca2+ concentration, and we therefore examined the effects of extracellular and intracellular acidosis on Ca2+ responses and EDRF production in cultured porcine aortic endothelial cells.

Methods and results

Cytosolic pH (pHi) and Ca2+ were measured using fluorescent dyes, BCECM/AM (pH-indicator) and fura-2/AM (Ca2+-indicator), respectively. EDRFs, nitric oxide (NO) and prostaglandin I2 (PGI2) were assessed using DAF-FM/DA (NO-indicator dye) fluorometry and 6-keto PGF1 enzyme immunoassay, respectively. HEPES buffers titrated to pH 6.4, 6.9, and 7.4 were used to alter extracellular pH (pHo), and propionate (20 mmol/L) was applied to cause intracellular acidosis. Extracellular acidosis strongly suppressed bradykinin (BK, 10 nmol/L)- and thapsigargin (TG, 1 µmol/L)-induced Ca2+ responses by 30 and 23% at pHo 6.9, and by 80 and 97% at pHo 6.4, respectively. During the examinations, there were no significant differences in pHi among the three groups at pHo 7.4, 6.9, and 6.4. Extracellular acidosis also inhibited BK-stimulated PGI2 production by 55% at pHo 6.9 and by 77% at pHo 6.4, and NO production by 38% at pHo 6.9 and by 91% at pHo 6.4. The suppressive effects of extracellular acidosis on Ca2+ responses and NO production were reversible. Propionate changed pHi from 7.3 to 6.9, without altering pHo (7.4). Intracellular acidosis had no effect on BK- and TG-induced Ca2+ responses or NO production.

Conclusion

These results indicate that extracellular, but not intracellular, acidosis causes endothelial dysfunction by inhibiting store-operated Ca2+ entry, so helping to clarify the vascular pathophysiology of conditions such as ischaemia, hypoxia, acidosis, and ischaemia-reperfusion.

  T Sawada , P. B Francisco , S Aihara , Y Utsumi , M Yoshida , Y Oyama , M Tsuzuki , H Satoh and Y. Nakamura
 

In monocots, starch branching enzyme II (BEII) was functionally differentiated into BEIIa and BEIIb after separation from the dicots, and in cereals BEIIb plays a distinct role in amylopectin biosynthesis in the endosperm. The present study was conducted to examine to what extent a green algal BEII has an overlapping function with BEIIb in starch biosynthesis by introducing the Chlorella BEII gene into an amylose-extender (ae) mutant of rice. Chlorella BEII was found to complement the contribution of the rice endosperm BEIIb to the structures of amylopectin and starch granules because these mutated phenotypes were recovered almost completely to those of the wild type by the expression of Chlorella BEII. When the recombinant BE enzymes were incubated with the rice ae amylopectin, the branching pattern of Chlorella BEII was much more similar to that of rice BEIIb rather than rice BEIIa. Detailed analyses of BE reaction products suggests that BEIIb and Chlorella BEII only transfer chains with a degree of polymerization (DP) of 6 and 7, whereas BEIIa preferably transfers short chains with a DP of about 6–11. These results show that the Chlorella BEII is functionally similar to rice BEIIb rather than BEIIa.

  T Takahashi , H Satoh , M Takaguchi , S Takafuji , H Yokoyama , S Fujii and T. Suzuki
 

Association of sulphatide with influenza A virus (IAV) haemagglutinin (HA) delivered to the cell surface promotes progeny virus production. However, it is not known whether there is direct binding of HA to sulphatide. In this study, we found that recombinant HA, which was produced by a baculovirus protein expression system from the HA gene of A/duck/HK/313/4/78 (H5N3), bound to sulphatide in a dose-dependent manner and that the binding was inhibited by a specific antibody. Our results indicate that the recombinant HA is useful for elucidation of the binding domain of HA with sulphatide and for the development of new anti-IAV agents.

 
 
 
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