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Articles by S Saito
Total Records ( 6 ) for S Saito
  T Wada , S Hori , M Sugiyama , E Fujisawa , T Nakano , H Tsuneki , K Nagira , S Saito and T. Sasaoka
 

Maternal insulin resistance is essential for efficient provision of glucose to the fetus. Although elevation of placental hormones is known to relate to the development of insulin resistance, the precise underlying mechanism of maternal insulin resistance is unknown. Therefore, we examined the molecular mechanisms of progesterone causing insulin resistance in 3T3-L1 adipocytes. Progesterone at 10–4 M, but not 10–5 M, reduced the amount of IRS-1. As a result, insulin-induced phosphorylation of IRS-1, the association of IRS-1 with p85, and subsequent phosphorylation of Akt1 and -2 was decreased moderately by 10–4 M progesterone. Subsequently, insulin-induced translocation of GLUT4 to the plasma membrane evaluated by immunostaining on the plasma membrane sheet by confocal laser microscope was also decreased by 10–4 M progesterone. In contrast, 2-[3H]deoxyglucose (2DG) uptake was markedly inhibited by both 10–5 and 10–4 M progesterone in a dose-dependent manner. Surprisingly, 2DG uptake elicited by adenovirus-mediated expression of constitutive-active mutant of PI 3-kinase (myr-p110) and Akt (myr-Akt) was suppressed by progesterone. Interestingly, insulin-induced tyrosine phosphorylation of Cbl and activation of TC10 were inhibited by progesterone at 10–5 M. These results indicate that progesterone is implicated in insulin resistance during pregnancy by inhibiting the PI 3-kinase pathway at the step of 1) IRS-1 expression and 2) distal to Akt and 3) by suppressing the PI 3-kinase-independent pathway of TC10 activation by affecting Cbl phosphorylation.

  Y Miyashita , S Saito , A Miyamoto , O Iida and S. Nanto
 

Skin perfusion pressure (SPP) is a measure of peripheral circulation; low SPP (<40 mm Hg) indicates poor wound healing. Cilostazol is used to alleviate symptoms and improve walking distance in patients with peripheral artery disease (PAD), but its effect on SPP is unknown. We enrolled patients whose symptoms were Rutherford class 3 or 4 and whose SPP was <40 mm Hg. We analyzed patient symptoms, ankle-brachial index (ABI), and SPP before and 1 month after treatment with cilostazol. We analyzed 20 legs of 14 patients. Cilostazol improved symptoms in 12 legs. The average heart rate increased from 76 ± 16 to 84 ± 20 beats/min (P < .05). Cilostazol did not increase the ABI but caused a significant increase in the SPP from 24.5 ± 8.88 to 42.8 ± 21.0 mm Hg (P < .01). Cilostazol increases microvascular circulation in severely ischemic limbs and may be useful in critical limb ischemia.

  A Abdel Nazeer , S Saito , S Sayed , L Hassan , F Askar , W Al jahdari , T Seki and O. Hideaki
  Background

Local anaesthetics exhibit direct neurotoxic effects on neurones. Numerous studies have investigated the factors that may reverse this neuropathology, but the effects of glucose conditions on neuronal regeneration after lidocaine-induced injury have not been examined by observing living neurones. The present study investigated the effects of different glucose conditions on neurite length, growth cone regeneration, and cell death in dorsal root ganglia (DRG) neurones after lidocaine-induced injury in vitro.

Methods

DRG explants were isolated from chick embryos at embryonic day 8 and cultured in media containing low, normal, or high glucose concentrations (10, 25, or 40 mM) for 24 h. Tissues were exposed to lidocaine 8 mM for 1 h, then rinsed and incubated for a further 24 h. Neurite length and growth cone collapse assays were performed to assess neuronal growth and regeneration. Lactate dehydrogenase (LDH) and caspase assays were also performed to detect neuronal cell death.

Results

Addition of lidocaine for 1 h resulted in >97% growth cone collapse and neurite destruction under all three glucose conditions. Two hours after rinsing out the lidocaine, significant reversal of growth cone collapse and neurite elongation was observed under all glucose conditions. Growth cone collapse was higher under low-glucose condition (P<0.05). High glucose negatively affected neurite length more than growth cone collapse. At 24 h, LDH release with both low- and high-glucose conditions was higher than with normal glucose (P<0.05). Low- and high-glucose conditions increased caspase 3/7 activation.

Conclusions

Normal glucose is optimal for neuronal recovery after lidocaine-induced injury in vitro.

  M Toyofuku , T Kimura , T Morimoto , Y Hayashi , H Ueda , K Kawai , Y Nozaki , S Hiramatsu , A Miura , Y Yokoi , S Toyoshima , H Nakashima , K Haze , M Tanaka , S Take , S Saito , T Isshiki , K Mitsudo and on Behalf of the j Cypher Registry Investigators
 

Background— Long-term outcomes after stenting of an unprotected left main coronary artery (ULMCA) with drug-eluting stents have not been addressed adequately despite the growing popularity of this procedure.

Methods and Results— j-Cypher is a multicenter prospective registry of consecutive patients undergoing sirolimus-eluting stent implantation in Japan. Among 12 824 patients enrolled in the j-Cypher registry, the unadjusted mortality rate at 3 years was significantly higher in patients with ULMCA stenting (n=582) than in patients without ULMCA stenting (n=12 242; 14.6% versus 9.2%, respectively; P<0.0001); however, there was no significant difference between the 2 groups in the adjusted risk of death (hazard ratio 1.23, 95% confidence interval 0.95 to 1.60, P=0.12). Among 476 patients whose ULMCA lesions were treated exclusively with a sirolimus-eluting stent, patients with ostial/shaft lesions (n=96) compared with those with bifurcation lesions (n=380) had a significantly lower rate of target-lesion revascularization for the ULMCA lesions (3.6% versus 17.1%, P=0.005), with similar cardiac death rates at 3 years (9.8% versus 7.6%, P=0.41). Among patients with bifurcation lesions, patients with stenting of both the main and side branches (n=119) had significantly higher rates of cardiac death (12.2% versus 5.5%; P=0.02) and target-lesion revascularization (30.9% versus 11.1%; P<0.0001) than those with main-branch stenting alone (n=261).

Conclusions— The higher unadjusted mortality rate of patients undergoing ULMCA stenting with a sirolimus-eluting stent did not appear to be related to ULMCA treatment itself but rather to the patients’ high-risk profile. Although long-term outcomes in patients with ostial/shaft ULMCA lesions were favorable, outcomes in patients with bifurcation lesions treated with stenting of both the main and side branches appeared unacceptable.

  Y Kawasaki , A Ito , D. A Withers , T Taima , N Kakoi , S Saito and Y. Arai
 

In renal cell carcinoma (RCC), the presence of higher gangliosides correlates with systematic metastasis. Disialosyl globopentaosylceramide (DSGb5) was identified previously as one of the major gangliosides from RCC tissues. Siglec-7 (sialic acid-binding Ig-like lectin-7), expressed on natural killer (NK) cells as an inhibitory receptor, has a striking preference for internally branched 2,6-linked disialic gangliosides such as DSGb5. To clarify the functional role of DSGb5 in RCC metastases, we have investigated whether DSGb5 expressed on RCC cells can modulate NK cell cytotoxicity in a Siglec-7-dependent manner. The binding activity of RCC cells to Siglec-7-Fc fusion protein was specifically inhibited by anti-DSGb5 monoclonal antibody and transfection of siRNA for ST6GalNAcVI (synthetase of DSGb5). These observations showed that Siglec-7-Fc fusion protein specifically bound to DSGb5 expressed on RCC cells. In contrast, the sialic acid-binding site of Siglec-7 on NK cells was masked by cis interactions with endogenous sialoconjugates at the cell surface, but it could be unmasked by sialidase treatment of the NK cells. Following sialidase treatment of NK cells, NK cell cytotoxicity against RCC cells with high DSGb5 expression was significantly decreased relative to cells with low DSGb5 expression. These findings indicate that such NK cell cytotoxicity against RCC cells could be inhibited by the interaction between Siglec-7 on effecter cells and DSGb5 on target cells. The results of the present study suggest that DSGb5 expressed on RCC cells can downregulate NK cell cytotoxicity in a DSGb5-Siglec-7-dependent manner and that RCC cells with DSGb5 create favorable circumstance for their own survival and metastases.

  S Takiya , S Saito , T Yokoyama , D Matsumoto , T Aizawa , M Kamiya , M Demura and K. Kawano
 

The STPR domain is a novel DNA-binding domain composed of repeats of 23 amino-acid-long peptide found in the fibroin-modulator-binding protein-1 (FMBP-1) of the silkworm Bombyx mori. Theoretical proteins having the STPR domain are highly conserved, particularly in vertebrates, but the functions are mostly unknown. In this study, the DNA-binding property of the STPR domain in FMBP-1 was examined. Use of reagents selecting the DNA groove and an oligonucleotide in which the dA:dT pairs of the probe were replaced with dI:dC pairs in mobility shift assay demonstrated that FMBP-1 approaches DNA from the major groove. Permutation electrophoresis using probes of the same length but containing the FMBP-1-binding site at different positions showed that FMBP-1 bends DNA through its binding. To induce the sharp bend of DNA, the STPR domain alone was insufficient and the long N-terminal extending region was necessary. Moreover, the basic region extending from the N-terminus of the STPR domain stabilized the DNA binding of the STPR domain. These results suggested that DNA-binding properties of the STPR domain are affected strongly by the structure of the flanking regions in the STPR domain-containing proteins.

 
 
 
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