Shigeru Oikawa

Kokushikan University, Edo, Tōkyō, Japan

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Publications (10)24.29 Total impact

  • Nihon Naika Gakkai Zasshi 02/2007; 96(1):150-2.
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    ABSTRACT: The mechanism of peritoneal fibrosis in patients on continuous ambulatory peritoneal dialysis (CAPD) is poorly elucidated. We investigated the cellular mechanism of high-glucose-induced expression of monocyte chemoattractant protein-1 (MCP-1), which is important in recruiting monocytes into the peritoneum and progression of peritoneal fibrosis, and examined the inhibitory mechanism of glucocorticoids. Rat peritoneal mesothelial cells were cultured in high-glucose-containing medium and then analyzed for phosphorylation levels of p42/44 and p38 mitogen-activated protein (MAP) kinases (MAPK), MAPK or extracellular signal-regulated kinase kinase (MEK)1/2, c-Jun N-terminal kinase (JNK)1/2, and protein kinase C (PKC) by Western blotting. Expression of MCP-1 was examined by reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. DNA-binding activity of nuclear factor (NF)-kappaB was measured by electrophoretic mobility shift assay. High glucose increased MCP-1 mRNA and MCP-1 protein expression. Although glucose increased phosphorylation of MEK1/2, p42/44 MAPK, p38 MAPK, JNK1/2, and PKC, and DNA-binding activity of NF-kappaB, its effect on MCP-1 expression was suppressed only by PKC and NF-kappaB inhibitors. Mannitol caused a similar increase in PKC and NF-kappaB activation and MCP-1 synthesis. Prednisolone increased I-kappaB-alpha expression and inhibited glucose/mannitol-induced NF-kappaB DNA binding and MCP-1 expression without affecting PKC phosphorylation. The inhibitory effects of prednisolone on MCP-1 expression were reversed by mifepristone, a glucocorticoid receptor antagonist. Our results indicate that glucose induces MCP-1 mainly through hyperosmolarity by activating PKC and its downstream NF-kappaB, and that such effect was inhibited by prednisolone, suggesting the efficacy of prednisolone in preventing peritoneal fibrosis in patients on CAPD.
    Kidney International 03/2006; 69(4):736-46. · 8.52 Impact Factor
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    ABSTRACT: The carotid bodies are enlarged in the rats exposed to long term hypoxia. In some studies the animals were exposed to hypoxia for relatively short periods, and in other studies for relatively long periods. However, most authors use the term “chronic hypoxia” in their publications. This terminology can cause much confusion. On the other hand, there are no morphological studies of the carotid bodies after the termination of chronic hypoxia except in a few instances (Heath et al., 1973). Recently high altitude training has been used to try to improve some physical conditions. High altitude exercise can help to make clear morphological changes in chemoreceptor organs during acclimatization to hypoxia and during deacclimatization after chronic hypoxia is terminated.
    Advances in experimental medicine and biology 02/2006; 580:49-54; discussion 351-9. · 1.83 Impact Factor
  • Advances in experimental medicine and biology 02/2006; 580:55-61; discussion 351-9. · 1.83 Impact Factor
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    ABSTRACT: Growth factors, extracellular matrix and its receptor integrins are upregulated in various glomerular diseases. We investigated the mechanism of collaboration between integrins and platelet-derived growth factor (PDGF) in focal adhesion kinase (FAK)- and extracellular signal-related kinase (ERK)1/2-mediated signal pathways that lead to monocyte chemoattractant protein (MCP)-1 expression in cultured rat mesangial cells (MCs). Serum-starved MCs were plated on fibronectin- or polylysine-coated plates with or without PDGF, and examined for phosphorylation of ERK1/2, mitogen-activated protein or ERK kinase (MEK)1/2 and FAK by western blotting, and for expression of MCP-1 mRNA and protein by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. The effects of dominant-negative FAK on MCP-1 expression were examined. Cell adhesion to fibronectin increased phosphorylation of FAK, MEK1/2 and ERK1/2, and induced MCP-1 mRNA and protein expression. PDGF increased phosphorylation of FAK, MEK1/2 and ERK1/2 even without cell adhesion to fibronectin, and induced MCP-1 mRNA and protein expression. PDGF with integrin activation by fibronectin synergistically increased phosphorylation of FAK, MEK1/2 and ERK1/2, and expression of MCP-1 mRNA and protein. Dominant-negative FAK attenuated fibronectin enhancement of PDGF-induced ERK1/2 phosphorylation and MCP-1 expression, indicating involvement of FAK in this signalling. Our results suggest the cooperative role of integrin and PDGF receptor in activation of the ERK pathway possibly via FAK in MCs. The synergistic activation of integrin and PDGF signalling may play an important role in the progression of glomerular diseases through the induction of MCP-1.
    Nephrology Dialysis Transplantation 11/2005; 20(10):2080-8. · 3.37 Impact Factor
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    ABSTRACT: The role of the autonomic nervous system, the central and peripheral chemoreceptors, and the arterial baroreceptors was examined in the cardiovascular response to hypercapnia in conscious rats chronically instrumented for the measurement of arterial blood pressure (ABP), heart rate (HR), and renal sympathetic nerve activity (RSNA). Rats were exposed to hypercapnia (6% CO2), and the cardiovascular and autonomic nervous responses in intact and carotid chemo- and/or aortic denervated rats were compared. In intact and carotid chemo-denervated rats, hypercapnia induced significant increases in mean ABP (MABP) and RSNA, and a significant decrease in HR. The HR decrease was reversed by atropine and eliminated by bilateral aortic denervation, which procedure, however, did not affect the MABP or RSNA response. Bilateral carotid chemo-denervation did not affect the baroreflex control of HR, although this control was attenuated by aortic denervation. Hypercapnia did not affect baroreflex sensitivity in intact rats. These results suggest that hypercapnia induces an increase in MABP due to an activation of sympathetic nervous system via central chemoreceptors and a decrease in HR due to a secondary reflex activation of the parasympathetic nervous system via arterial baroreceptors in response to the rise in ABP. In addition, carotid chemoreceptors do not play a major role in the overall cardiovascular response to hypercapnia in conscious rats. The mechanism responsible for the parasympatho-excitation may also involve CO2 induced aortic chemoreceptor simulation.
    Autonomic Neuroscience 03/2005; 117(2):105-14. · 1.85 Impact Factor
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    ABSTRACT: Morphological changes in the rat carotid bodies 1, 2, 4, and 8 weeks after the termination of chronically hypocapnic hypoxia (10% O2 for 8 weeks) were examined by means of morphometry and immunohistochemistry. The rat carotid bodies after 8 weeks of hypoxic exposure were enlarged several fold with vascular expansion. The carotid bodies 1 and 2 weeks after the termination of 8 weeks of hypoxic exposure were diminished in size, although their diameter remained larger than the normoxic controls. The expanded vasculature in chronically hypoxic carotid bodies returned to the normoxic control state. In the carotid bodies 1 week after the termination of chronic hypoxia, the density of NPY fibers was remarkably increased and that of VIP fibers was dramatically decreased in comparison with the density in chronically hypoxic carotid bodies. In the carotid bodies 2 and 4 weeks after the termination of hypoxia, the density of SP and CGRP fibers was gradually increased. In the carotid bodies 8 weeks after the termination of hypoxia, the appearance of the carotid body returned to a nearly normoxic state, and the density of SP, CGRP, VIP, and NPY fibers also recovered to that of normoxic controls. These results suggest that the morphological changes in the recovering carotid bodies start at a relatively early period after the termination of chronic hypoxia, and a part of these processes may be under the control of peptidergic innervation.
    Histology and histopathology 11/2004; 19(4):1133-40. · 2.28 Impact Factor
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    ABSTRACT: Elevated parathyroid hormone (PTH) levels and hyperphosphatemia are thought to be associated with the development of calciphylaxis. We report a patient on hemodialysis who developed proximal calciphylaxis with consistently low PTH levels after parathyroidectomy. A 31-year-old man was admitted to our hospital because of abdominal skin ulcerations. Calciphylaxis spread to the penis, and simultaneous progressive lung calcification was evident on chest X-ray, suggestive of pulmonary calciphylaxis on 99mTc-methylene disphosphonate scintigraphy. The patient died of respiratory failure despite intensive treatment including hyperbaric oxygen therapy. This is the first report of a patient on hemodialysis who developed calciphylaxis involving the penis after parathyroidectomy.
    Internal Medicine 02/2004; 43(1):63-8. · 0.97 Impact Factor
  • Advances in experimental medicine and biology 02/2003; 536:455-60. · 1.83 Impact Factor
  • Advances in experimental medicine and biology 02/2003; 536:473-9. · 1.83 Impact Factor

Publication Stats

46 Citations
24.29 Total Impact Points

Institutions

  • 2006
    • Kokushikan University
      Edo, Tōkyō, Japan
  • 2003–2004
    • University of Occupational and Environmental Health
      • • School of Medicine
      • • Department of Systems Physiology
      Kitakyūshū, Fukuoka-ken, Japan