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Articles by Y Okada
Total Records ( 3 ) for Y Okada
  M Ishida , S Mikami , E Kikuchi , T Kosaka , A Miyajima , K Nakagawa , M Mukai , Y Okada and M. Oya

Aryl hydrocarbon receptor (AhR) and the activation of the AhR pathway are involved in xenobiotic-induced toxicity and carcinogenesis. Although xenobiotics, such as cigarette smoke, contribute to the development of urothelial carcinoma (UC), the relationship between AhR and UC is unclear. In the present study, we investigated AhR expression in 209 patients with upper urinary tract UC. The nuclear expression of AhR was significantly associated with histological grade, pathological T stage, lymphovascular invasion and lymph node involvement. A multivariate Cox analysis revealed that nuclear AhR expression was a significant and independent predictor for disease-specific survival (hazard ratio = 2.469, P = 0.013). To determine whether the AhR pathway can be activated in the T24 UC cell line, we examined the expression of cytochrome P450 (CYP) 1A1 and CYP1B1, which are target genes of the AhR pathway, following exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a ligand of AhR. TCDD treatment upregulated the expression levels of AhR, CYP1A1 and CYP1B1. TCDD enhanced T24 cell invasion associated with the upregulation of matrix metalloproteinase (MMP)-1 and MMP-9. Furthermore, targeting AhR messenger RNA (mRNA) expression in T24 cells with small interfering RNA (siRNA) downregulated the mRNA expression of AhR, CYP1A1, CYP1B1, MMP-1, MMP-2 and MMP-9; furthermore, the cells transfected with siRNA for AhR showed decreased invasion activity in comparison with the cells transfected with a non-targeting siRNA. Our results therefore suggest that AhR plays a role in the invasiveness of UC cells and can serve as a marker for the prognosis of upper urinary tract UC.

  T Sato , K Nishishita , Y Okada and K. Toda

Temperature sensitivity of frog taste cells was studied. The taste cell designated Type thermosensitive (TS) I cell was depolarized by warm stimulus at 30 °C and hyperpolarized by cold stimulus at 10 °C. The taste cell designated Type TS II cell was depolarized by the cold stimulus and hyperpolarized by the warm stimulus. Menthol solution at 20 °C, which selectively activates transient receptor potential (TRP) M8 channels sensitive to cold stimuli, depolarized Type TS II cells but not Types TS I cells. Thermal stimuli–induced receptor potentials were all blocked by a nonselective cation channel blocker flufenamic acid. The results indicate that Type TS I cells have warm sensor channels alone, Type TS II cells have cold sensor channels alone and both the channels are a nonselective cation channel. The candidate of cold sensor channel in Type TS II cells is a TRPM8 channel and that of warm sensor channel in Type TS I cells is likely to be a TRPM4-like channel from the published data. In a subset of taste cells, Types TS III and TS IV cells were found. The former was depolarized by both cold and warm stimuli, but the latter was hyperpolarized by both stimuli. Types TS III and TS IV cells might have both TRPM4-like and TRPM8 channels. It is supposed that depolarizations induced by both cold and warm stimuli were dominant in Type TS III cells and hyperpolarizations induced by both the thermal stimuli were dominant in Type TS IV cells.

  H Inoue , N Takahashi , Y Okada and M. Konishi

The volume-sensitive outwardly rectifying (VSOR) chloride channel is ubiquitously expressed and involved in cell volume regulation after osmotic swelling, called regulatory volume decrease (RVD), in various cell types. In adipocytes, the expression of the VSOR channel has not been explored to date. Here, by employing the whole-cell patch-clamp technique, we examined whether or not the VSOR channel is expressed in white adipocytes freshly isolated from epididymal fat pads of normal (C57BL/6 or KK) and diabetic (KKAy) mice. Whole cell voltage-clamp recordings revealed that Cl currents were gradually activated upon cell swelling induced by application of a hypotonic solution, both in normal and diabetic adipocytes. Although both the mean cell size (or cell capacitance) and the current magnitude in KKAy adipocytes were larger than those in C57BL/6 cells, the current density was significantly lower in KKAy adipocytes (23.32 ± 1.94 pA in C57BL/6 adipocytes vs. 13.04 ± 2.41 pA in KKAy adipocytes at +100 mV). Similarly, the current density in diabetic KKAy adipocytes was lower than that in adipocytes from KK mice (a parental strain of KKAy mice), which do not present diabetes until an older age. The current was inhibited by Cl channel blockers, 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB) and glibenclamide, or hypertonic solution, and showed outward rectification and inactivation kinetics at large positive potentials. These electrophysiological and pharmacological properties are consistent with those of the VSOR channel in other cell types. Moreover, adipocytes showed RVD, which was inhibited by NPPB. In KKAy adipocytes, RVD was significantly slower (; 8.42 min in C57BL/6 adipocytes vs. 11.97 min in KKAy adipocytes) and incomplete during the recording period (25 min). It is concluded that the VSOR channel is functionally expressed and involved in volume regulation in white adipocytes. RVD is largely impaired in adipocytes from diabetic mice, presumably as a consequence of the lower density of the functional VSOR channel in the plasma membrane.

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