Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where Shoji Kagami is active.

Publication


Featured researches published by Shoji Kagami.


Nature Genetics | 2001

Mutation of DNASE1 in people with systemic lupus erythematosus.

Koji Yasutomo; Takahiko Horiuchi; Shoji Kagami; Hiroshi Tsukamoto; Chinami Hashimura; Maki Urushihara; Yasuhiro Kuroda

Systemic lupus erythematosus (SLE) is a highly prevalent human autoimmune diseases that causes progressive glomerulonephritis, arthritis and an erythematoid rash. Mice deficient in deoxyribonuclease I (Dnase1) develop an SLE-like syndrome. Here we describe two patients with a heterozygous nonsense mutation in exon 2 of DNASE1, decreased DNASE1 activity and an extremely high immunoglobulin G titer against nucleosomal antigens. These data are consistent with the hypothesis that a direct connection exists between low activity of DNASE1 and progression of human SLE.


Hypertension | 2004

Possible Contributions of Reactive Oxygen Species and Mitogen-Activated Protein Kinase to Renal Injury in Aldosterone/Salt-Induced Hypertensive Rats

Akira Nishiyama; Li Yao; Yukiko Nagai; Kayoko Miyata; Masanori Yoshizumi; Shoji Kagami; Shuji Kondo; Hideyasu Kiyomoto; Takatomi Shokoji; Shoji Kimura; Masakazu Kohno; Youichi Abe

Abstract—Studies were performed to test the hypothesis that reactive oxygen species (ROS) and mitogen-activated protein kinase (MAPK) contribute to the pathogenesis of aldosterone/salt-induced renal injury. Rats were given 1% NaCl to drink and were treated with one of the following combinations for 6 weeks: vehicle (0.5% ethanol, SC, n=6); aldosterone (0.75 &mgr;g/H, SC, n=8); aldosterone plus a selective mineralocorticoid receptor antagonist; eplerenone (0.125% in chow, n=8); aldosterone plus an antioxidant; and tempol (3 mmol/L in drinking solution, n=8). The activities of MAPKs, including extracellular signal-regulated kinases (ERK)1/2, c-Jun-NH2-terminal kinases (JNK), p38MAPK, and big-MAPK-1 (BMK1) in renal cortical tissues were measured by Western blot analysis. Aldosterone-infused rats showed higher systolic blood pressure (165±5 mm Hg) and urinary excretion of protein (106±24 mg/d) than vehicle-infused rats (118±3 mm Hg and 10±3 mg/d). Renal cortical mRNA expression of p22phox, Nox-4, and gp91phox, measured by real-time polymerase chain reaction, was increased in aldosterone-infused rats by 2.3, 4.3, and 3.0-fold, respectively. Thiobarbituric acid-reactive substances (TBARS) content in renal cortex was also higher in aldosterone (0.23±0.02) than vehicle-infused rats (0.09±0.01 nmol/mg protein). ERK1/2, JNK, and BMK1 activities were significantly elevated in aldosterone-infused rats by 3.3, 2.3, and 3.0-fold, respectively, whereas p38MAPK activity was not changed. Concurrent administration of eplerenone or tempol to aldosterone-infused rats prevented the development of hypertension (127±2 and 125±5 mm Hg), and the elevations of urinary excretion of protein (10±2 and 9±2 mg/day) or TBARS contents (0.08±0.01 and 0.11±0.01 nmol/mg protein). Furthermore, eplerenone and tempol treatments normalized the activities of ERK1/2, JNK, and BMK1. These data suggest that ROS and MAPK play a role in the progression of renal injury induced by chronic elevations in aldosterone.


Annals of the Rheumatic Diseases | 2007

Genetic variations of Toll-like receptor 9 predispose to systemic lupus erythematosus in Japanese population

Kayoko Tao; Mutsuko Fujii; Shin Ichi Tsukumo; Yoichi Maekawa; Kenji Kishihara; Yasutaka Kimoto; Takahiko Horiuchi; Hajime Hisaeda; Shizuo Akira; Shoji Kagami; Koji Yasutomo

Background: Systemic lupus erythematosus (SLE) is characterised by dysregulation of autoreactive lymphocytes and antigen-presenting cells. Signalling through Toll-like receptor 9 (TLR9), a mediator of innate immune responses, has a role in activation of dendritic cells and autoreactive B cells. Objective: To investigate whether TLR9 polymorphisms are associated with an increased risk of SLE. Methods: DNA samples were obtained from 220 Japanese patients with SLE (with >4 American College of Rheumatology criteria for SLE) and 203 controls. The genetic variations of TLR9 were detected by PCR, followed by DNA sequencing. The promoter and enhancer activities of TLR9 were measured by luciferase reporter gene assay. The titres of anti-dsDNA antibodies in sera from control or TLR9-deficient mice were analysed by ELISA. Results: The G allele at position +1174 (located in intron 1 of TLR9) is closely associated with an increased risk of SLE (p = 0.029). Furthermore, patients with SLE tend to have C allele at position −1486 (p = 0.11). Both alleles down regulate TLR9 expression by reporter gene assay. TLR9-deficient mice under a C57BL/6 background possess higher titres of anti-dsDNA serum antibodies than control C57BL/6 mice. Conclusions: These results indicate that the presence of the G allele at position +1174 of TLR9 predisposes humans to an increased risk of SLE. It is speculated that TLR9 normally prevents the development of human SLE.


The American Journal of the Medical Sciences | 2009

Increased Urinary Angiotensinogen Is Precedent to Increased Urinary Albumin in Patients With Type 1 Diabetes

Toshie Saito; Hiroyuki Kobori; Maki Urushihara; Yumiko Kotani; Shoji Kagami

Background:We previously reported that kidney and urinary angiotensinogen levels were significantly increased before the development of diabetic nephropathy in diabetic rats. To address this system in humans, we have developed an enzyme-linked immunosorbent assay for human angiotensinogen and reported that urinary excretion of angiotensinogen levels is enhanced in patients with chronic kidney disease, including patients with type 2 diabetes. On the basis of these findings, this study was performed to demonstrate that urinary angiotensinogen levels increased before the onset of microalbuminuria and that urinary angiotensinogen can be an early biomarker of intrarenal renin-angiotensin system status in normoalbuminuric patients with type 1 diabetes compared with age- and sex-matched control subjects. Methods:The study included 28 patients with type 1 diabetes and 21 control subjects. No subject received renin-angiotensin system blockades. Random spot urine samples as well as blood samples were obtained and analyzed. Results:Urinary albumin:creatinine ratio or urinary protein:creatinine ratio did not increase in patients compared with control subjects, suggesting that these patients were in their premicroalbuminuric phase of diabetic nephropathy. However, the urinary angiotensinogen:creatinine ratio was significantly higher in patients than in control subjects (12.1 ± 3.2 &mgr;g/g versus 4.2 ± 0.7 &mgr;g/g). Importantly, an increase in plasma angiotensinogen levels was not observed (26.3 ± 1.3 &mgr;g/mL versus 29.5 ± 3.3 &mgr;g/mL). Conclusions:Thus, in patients, an increase in urinary angiotensinogen levels is observed, and this increase is precedent to an increase in urinary albumin levels, suggesting that urinary angiotensinogen may function as an early marker of diabetic nephropathy.


British Journal of Pharmacology | 2002

Ebselen attenuates oxidative stress-induced apoptosis via the inhibition of the c-Jun N-terminal kinase and activator protein-1 signalling pathway in PC12 cells.

Masanori Yoshizumi; Toshiaki Kogame; Yuki Suzaki; Yoshiko Fujita; Moe Kyaw; Kazuyoshi Kirima; Keisuke Ishizawa; Koichiro Tsuchiya; Shoji Kagami; Toshiaki Tamaki

Ebselen (2‐phenyl‐1,2‐benzisoselenazol‐3[2H]‐one) is a selenoorganic compound exhibiting both glutathione peroxidase activity and antioxidant activity. Although it has been reported that ebselen is effective for oxidative stress‐induced neuronal damage both in vivo and clinically, the precise mechanisms of the efficacy have not yet been elucidated. Thus, we hypothesized that ebselen may affect reactive oxygen species‐induced mitogen‐activated protein (MAP) kinase activation in cultured PC12 cells. Our findings showed that hydrogen peroxide (H2O2) stimulated rapid and significant activation of extracellular signal‐regulated kinase (ERK)1/2, c‐Jun N‐terminal kinase (JNK) and p38 in PC12 cells, which is a model of catecholamine‐containing neurons. H2O2‐induced JNK activation was inhibited by ebselen, whereas ERK1/2 and p38 activation by H2O2 were not affected by ebselen. Inhibition by ebselen of H2O2‐induced hydroxyl radical generation in PC12 cells was observed using electron paramagnetic resonance measurements. Ebselen also inhibited H2O2‐induced increases in DNA binding activity of activator protein‐1 (AP‐1), a downstream transcription factor of JNK, composed of the c‐Jun homo/heterodimer. Finally, pretreatment of cells with ebselen resulted in a significant recovery from cell death including apoptosis by H2O2 in PC12 cells. These findings suggest that ebselen attenuates oxidative stress‐induced neuronal cell death through the inhibition of the JNK and AP‐1 signalling pathway. Thus, inhibition of JNK by ebselen may imply its usefulness for treatment of ischaemic cerebral diseases relevant to neuronal cell death.


Vox Sanguinis | 2005

Factors associated with granulocyte colony-stimulating factor-induced peripheral blood stem cell yield in healthy donors

Hiroko Suzuya; Tsutomu Watanabe; Ryuji Nakagawa; Hiroyoshi Watanabe; Yasuhiro Okamoto; Toshihiro Onishi; Takanori Abe; Yoshifumi Kawano; Shoji Kagami; Yoichi Takaue

Background and Objectives  Poor collection results are a clinical problem in granulocyte‐colony stimulating factor (G‐CSF)‐induced peripheral blood stem cell (PBSC) collection in healthy donors. It would be beneficial to be able to predict the PBSC yield from allogeneic donors before mobilization or harvesting.


Journal of The American Society of Nephrology | 2004

The SOD mimetic tempol ameliorates glomerular injury and reduces mitogen-activated protein kinase activity in Dahl salt-sensitive rats.

Akira Nishiyama; Masanori Yoshizumi; Hirofumi Hitomi; Shoji Kagami; Shuji Kondo; Akira Miyatake; Megumu Fukunaga; Toshiaki Tamaki; Hideyasu Kiyomoto; Masakazu Kohno; Takatomi Shokoji; Shoji Kimura; Youichi Abe

It was shown recently that renal injury in Dahl salt-sensitive (DS) hypertensive rats is accompanied by mitogen-activated protein kinase (MAPK) activation. The present study was conducted to elucidate the contribution of reactive oxygen species to MAPK activities and renal injury in DS rats. DS rats were maintained on high salt (H; 8.0% NaCl; n = 7) or low salt (L; 0.3% NaCl; n = 6) diets; H + a superoxide dismutase mimetic, tempol (3 mmol/L in drinking water; n = 8); or H + hydralazine (0.5 mmol/L in drinking water; n = 8) for 4 wk. Mean BP (MBP) in DS/H and DS/L rats was 185 +/- 7 and 113 +/- 3 mmHg, respectively. DS/H rats showed a higher ratio of urinary protein excretion and creatinine (U(protein)V/U(cr)V; 20.3 +/- 1.1) and a higher cortical collagen content (22 +/- 1 micro g/mg) than in DS/L rats (2.4 +/- 0.1 and 13 +/- 1 micro g/mg, respectively). The expression of p22-phox and Nox-1, essential components of NAD(P)H oxidase, in renal cortical tissue was approximately threefold higher in DS/H rats than in DS/L rats. Increased activities of renal cortical MAPK, including extracellular signal-regulated kinases (ERK) 1/ERK2 and c-Jun NH(2)-terminal kinases (JNK) were also observed in DS/H rats by 7.0 +/- 0.7- and 4.3 +/- 0.2-fold, respectively. Tempol treatment significantly decreased MBP (128 +/- 3 mmHg), U(protein)V/U(cr)V (4.8 +/- 0.4), and cortical collagen content (14 +/- 1 micro g/mg) and normalized ERK1/ERK2 and JNK activities in DS/H rats. Histologically, tempol markedly ameliorated progressive sclerotic and proliferative glomerular changes in DS/H rats. Hydralazine-treated DS/H rats showed similar MBP (127 +/- 5 mmHg) to tempol-treated DS/H rats. Hydralazine also decreased U(protein)V/U(cr)V (16.2 +/- 1.5) and cortical collagen content (19 +/- 1 micro g/mg) in DS/H rats. However, these values were significantly higher than those of tempol-treated rats. Furthermore, although hydralazine significantly reduced JNK activity (-56 +/- 3%), ERK1/ERK2 activities were unaffected. These data suggest that reactive oxygen species, generated by NAD(P)H oxidase, contribute to the progression of renal injury through ERK1/ERK2 activation in DS/H hypertensive rats.


British Journal of Pharmacology | 1998

Effect of endothelin‐1 (1‐31) on extracellular signal‐regulated kinase and proliferation of human coronary artery smooth muscle cells

Masanori Yoshizumi; Shokei Kim; Shoji Kagami; Akinori Hamaguchi; Koichiro Tsuchiya; Hitoshi Houchi; Hiroshi Iwao; Hiroshi Kido; Toshiaki Tamaki

1 We have previously found that human chymase cleaves big endothelins (ETs) at the Tyr31‐Gly32 bond and produces 31‐amino acid ETs (1‐31), without any further degradation products. In this study, we investigated the effect of synthetic ET‐1 (1‐31) on the proliferation of cultured human coronary artery smooth muscle cells (HCASMCs). 2 ET‐1 (1‐31) increased [3H]‐thymidine incorporation and cell numbers to a similar extent as ET‐1 at 100 nM. This ET‐1 (1‐31)‐induced [3H]‐thymidine uptake was not affected by phosphoramidon, an inhibitor of ET‐converting enzyme. It was, however, inhibited by BQ123, an endothelin ETA receptor antagonist, but not by BQ788, an endothelin ETB receptor antagonist. 3 By using an in‐gel kinase assay, we demonstrated that ET‐1 (1‐31) activated extracellular signal‐regulated kinase 1/2 (ERK1/2) in a concentration‐dependent manner (100 pM to 1 μM) in HCASMCs. ET‐1 (1‐31)‐induced ERK1/2 activation was inhibited by BQ123, but not by BQ788 and phosphoramidon. Inhibition of protein kinase C (PKC) and ERK kinase also caused a reduction of ET‐1 (1‐31)‐induced ERK1/2 activation, whereas tyrosine kinase inhibition had little effect. 4 Gel‐mobility shift analysis revealed that the ERK1/2 activation was followed by an increase in transcription factor activator protein‐1 DNA binding activity in HCASMCs. 5 Our results strongly suggest that ET‐1 (1‐31) itself stimulates HCASMC proliferation probably through endothelin ETA or ETA‐like receptors. The underlining mechanism of cell growth by ET‐1 (1‐31) may be explained in part by PKC‐dependent ERK1/2 activation. Since human chymase has been proposed to play a role in atherosclerosis, ET‐1 (1‐31) may be one of the mediators.


American Journal of Nephrology | 2010

Urinary Angiotensinogen Accurately Reflects Intrarenal Renin-Angiotensin System Activity

Maki Urushihara; Shuji Kondo; Shoji Kagami; Hiroyuki Kobori

Background: We recently reported that immunoreactivity of intrarenal angiotensinogen (AGT) is significantly increased in IgA nephropathy patients. Meanwhile, we have developed direct enzyme-linked immunosorbent assays to measure plasma and urinary AGT (UAGT) in humans. This study was performed to test the hypothesis that UAGT levels are increased in chronic glomerulonephritis patients. Methods: We analyzed 100 urine samples from 70 chronic glomerulonephritis patients (26 from IgA nephropathy, 24 from purpura nephritis, 8 from lupus nephritis, 7 from focal segmental glomerulosclerosis, and 5 from non-IgA mesangial proliferative glomerulonephritis) and 30 normal control subjects. Results: UAGT–creatinine ratio (UAGT/UCre) was correlated positively with diastolic blood pressure (p = 0.0326), urinary albumin–creatinine ratio (p < 0.0001), urinary protein–creatinine ratio (p < 0.0001) and urinary occult blood (p = 0.0094). UAGT/UCre was significantly increased in chronic glomerulonephritis patients not treated with renin-angiotensin system (RAS) blockers compared with control subjects (p < 0.0001). Importantly, glomerulonephritis patients treated with RAS blockers had a marked attenuation of this augmentation (p = 0.0021). Conclusion: These data indicate that UAGT are increased in chronic glomerulonephritis patients and treatment with RAS blockers suppressed UAGT. The efficacy of RAS blockade to reduce the intrarenal RAS activity can be confirmed by measurement of UAGT in chronic glomerulonephritis patients.


Clinical and Experimental Nephrology | 2011

Japan renal biopsy registry: The first nationwide, web-based, and prospective registry system of renal biopsies in Japan

Hitoshi Sugiyama; Hitoshi Yokoyama; Hiroshi Sato; Takao Saito; Yukimasa Kohda; Shinichi Nishi; Kazuhiko Tsuruya; Hideyasu Kiyomoto; Hiroyuki Iida; Tamaki Sasaki; Makoto Higuchi; Motoshi Hattori; Kazumasa Oka; Shoji Kagami; Michio Nagata; Tetsuya Kawamura; Masataka Honda; Yuichiro Fukasawa; Atsushi Fukatsu; Kunio Morozumi; Norishige Yoshikawa; Yukio Yuzawa; Seiichi Matsuo; Yutaka Kiyohara; Kensuke Joh; Takashi Taguchi; Hirofumi Makino

BackgroundThe Committee for the Standardization of Renal Pathological Diagnosis and the Working Group for Renal Biopsy Database of the Japanese Society of Nephrology started the first nationwide, web-based, and prospective registry system, the Japan Renal Biopsy Registry (J-RBR), to record the pathological, clinical, and laboratory data of renal biopsies in 2007.MethodsThe patient data including age, gender, laboratory data, and clinical and pathological diagnoses were recorded on the web page of the J-RBR, which utilizes the system of the Internet Data and Information Center for Medical Research in the University Hospital Medical Information Network. We analyzed the clinical and pathological diagnoses registered on the J-RBR in 2007 and 2008.ResultsData were collected from 818 patients from 18 centers in 2007 and 1582 patients from 23 centers in 2008, including the affiliated hospitals. Renal biopsies were obtained from 726 native kidneys (88.8%) and 92 renal grafts (11.2%) in 2007, and 1400 native kidneys (88.5%) and 182 renal grafts (11.5%) in 2008. The most common clinical diagnosis was chronic nephritic syndrome (47.4%), followed by nephrotic syndrome (16.8%) and renal transplantation (11.2%) in 2007. A similar frequency of the clinical diagnoses was recognized in 2008. Of the native kidneys, the most frequent pathological diagnosis as classified by pathogenesis was immunoglobulin (Ig) A nephropathy (IgAN) both in 2007 (32.9%) and 2008 (30.2%). Among the primary glomerular diseases (except IgAN), membranous nephropathy (MN) was the most common disease both in 2007 (31.4%) and 2008 (25.7%).ConclusionsIn a cross-sectional study, the J-RBR has shown IgAN to be the most common disease in renal biopsies in 2007 and 2008, consistent with previous Japanese studies. MN predominated in the primary glomerular diseases (except for IgAN). The frequency of the disease and the clinical and demographic correlations should be investigated in further analyses by the J-RBR.

Collaboration


Dive into the Shoji Kagami's collaboration.

Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Shuji Kondo

University of Tokushima

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Miho Sakata

University of Tokushima

View shared research outputs
Top Co-Authors

Avatar

Miki Inoue

University of Tokushima

View shared research outputs
Top Co-Authors

Avatar

Kaname Okada

University of Tokushima

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Kenji Mori

University of Tokushima

View shared research outputs
Top Co-Authors

Avatar
Researchain Logo
Decentralizing Knowledge