研究者詳細 - 丸山　彰一

論文 - 丸山　彰一

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Overexpression of Calmodulin in Pancreatic {beta} Cells Induces Diabetic Nephropathy. 査読有り

Yuzawa Y, Niki I, Kosugi T, Maruyama S, Yoshida F, Takeda M, Tagawa Y, Kaneko Y, Kimura T, Kato N, Yamamoto J, Sato W, Nakagawa T, Matsuo S.

Journal of the American Society of Nephrology 19 巻 ( 9 ) 頁： 1701 - 1711 2008年

Cilostazol Improves Long-Term Patency after Percutaneous Transluminal Angioplasty in Hemodialysis Patients with Peripheral Artery Disease. 査読有り

Ishii H, Kumada Y, Toriyama T, Aoyama T, Takahashi H, Yamada S, Yasuda Y, Yuzawa Y, Maruyama S, Matsuo S, Matsubara T, Murohara T.

Clinical journal of the American Society of Nephrology 3 巻 ( 4 ) 頁： 1034 - 1040 2008年

Mineralocorticoid receptor blockade ameliorates peritoneal fibrosis in new rat peritonitis model. 査読有り

Nishimura H, Ito Y, Mizuno M, Tanaka A, Morita Y, Maruyama S, Yuzawa Y, Matsuo S.

American journal of physiology. Renal physiology 294 巻 ( 5 ) 頁： F1084 - 1093 2008年

Sirolimus-eluting stents vs bare metal stents for coronary intervention in Japanese patients with renal failure on hemodialysis. 査読有り

Aoyama T, Ishii H, Toriyama T, Takahashi H, Kasuga H, Murakami R, Amano T,Uetani T, Yasuda Y, Yuzawa Y, Maruyama S, Matsuo S, Matsubara T, Murohara T

Circulation journal 72 巻 ( 1 ) 頁： 56 - 60 2008年

High mobility group box chromosomal protein 1 in patients with renal diseases. 査読有り

Fumihiko Sato, Shoichi Maruyama, Hiroki Hayashi, Izumi Sakamoto, Shingo Yamada, Tomonori Uchimura, Yoshiki Morita, Yasuhiko Ito, Yukio Yuzawa, Ikuro Maruyama, Seiichi Matsuo

Nephron Clinical Practice 108 巻 ( 3 ) 頁： c194 - c201 2008年

Lipid droplet-associated proteins protect renal tubular cells from fatty acid-induced apoptosis. 査読有り

Urahama Y, Ohsaki Y, Fujita Y,Maruyama S, Yuzawa Y, Matsuo S, Fujimoto T.

Ameircan journal of Pathology 173 巻 ( 5 ) 頁： 1286 - 1294 2008年

Alternative strategy for overcoming ABO incompatibility. 査読有り

Kobayashi T, Liu D, Ogawa H, Miwa Y, Nagasaka T, Maruyama S, Li YT, Onishi A, Kuzuya T, Kadomatsu K, Uchida K, Nakao A.

Transplantation. 83 巻 ( 9 ) 頁： 1284 - 1286 2007年5月

Efficacy of oral nicorandil in patients with end-stage renal disease: a retrospective chart review after coronary angioplasty in Japanese patients receiving hemodialysis. 査読有り

Ishii H, Toriyama T, Aoyama T, Takahashi H, Yamada S, Kasuga H, Ichimiya S, Kanashiro M, Mitsuhashi H, Maruyama S, Matsuo S, Naruse K, Matsubara T, Murohara T.

Clin Ther. 29 巻 ( 1 ) 頁： 110 - 122 2007年1月

記述言語：英語掲載種別：研究論文（学術雑誌）

BACKGROUND: Patients receiving hemodialysis for end-stage renal disease (ESRD) are at high risk for death from ischemic heart disease (IHD). Nicorandil, a hybrid compound of adenosine triphosphate-sensitive potassium channel opener and nitric oxide donor, has been reported to improve the clinical prognosis of patients with IHD. OBJECTIVE: This study sought to investigate the efficacy of oral nicorandil in reducing the risks for cardiovascular events (CVEs) and CVE-related death in patients receiving hemodialysis for ESRD after undergoing percutaneous coronary intervention (PCI) for angina pectoris. METHODS: For this retrospective chart review, we used data from telephone interviews and medical charts from 3 hospitals in Japan. Data from patients aged <80 years who were receiving hemodialysis for ESRD and who had undergone successful PCI for angina between January 1999 and December 2004 were included in the analysis. Patients were stratified based on status of nicorandil treatment before PCI, as follows: patients receiving nicorandil 5 mg PO TID (the recommended dosage in Japan) for >1 month before PCI (nicorandil group) or those who did not receive nicorandil (control group). We investigated 6-year follow-up data on the primary end point, defined as CVEs (ie, unplanned hospital admission for worsening anginal status, or CVE-related death). The secondary end point was CVE-related death. After the data were initially analyzed, we performed a propensity-matched analysis to minimize selection bias. RESULTS: Data from 356 patients were included in the study (235 men, 121 women; mean [SD] age, 69 [9] years; mean [SD] weight, 52.3 [9.1] kg; nicorandil group, 198 patients; control group, 158 patients). According to the estimated propensity scores, 107 patients from each group were matched. There were no differences between the 2 groups in the baseline characteristics. On propensity-matched patient analysis, the estimated rates of patients who were CVE-free at 6 years were 3

DOI： 10.1016/j.clinthera.2007.12.020

PubMed

Relation between human decay-accelerating factor (hDAF) expression in pig cells and inhibition of human serum anti-pig cytotoxicity: value of highly expressed hDAF for xenotransplantation. 査読有り

Liu D, Kobayashi T, Onishi A, Furusawa T, Iwamoto M, Suzuki S, Miwa Y, Nagasaka T, Maruyama S, Kadomatsu K, Uchida K, Nakao A.

Xenotransplantation. 14 巻 ( 1 ) 頁： 67 - 73 2007年1月

記述言語：英語掲載種別：研究論文（学術雑誌）

BACKGROUND: Although the successful production of alpha1,3-galactosyltransferase-knockout (GT-KO) pigs has increased expectations of clinical xenotransplantation, additional modifications of genetically engineered pigs are still being explored, because even GT-KO pigs are incapable of inhibiting the host's immunological response completely. One of the potential candidates is a complement-regulatory protein, such as human decay-accelerating factor (hDAF). However, there are few reports on how high the expression level of hDAF in pig cells would be required for suppression of complement activation. The purpose of this study was to examine the relationship between the level of hDAF expression and its inhibitory effect on human serum cytotoxicity. METHODS: An expression (pCAGGS) vector containing the hDAF gene was transfected into pig fibroblasts using an electroporation system (Gene Pulser II). Forty-eight to fifty-two hours after transfection, the cells were stained with FITC-labeled anti-hDAF antibody and then applied to the cell sorter. hDAF-transfected cells with various expression levels were collected by gating on fluorescence intensity. The level of hDAF expression was determined relative to that in human control endothelial cells. Collected cells expressing x1, x5, x10, x15 and x30 hDAF were incubated into 96-well plates for 16 h, and the cells were subjected to 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl tetrazolium bromide (MTT) assay. RESULTS: hDAF expression levels in transfected cells at the time of MTT assay (16 h after sorting) were comparable to those immediately after sorting. hDAF expression in pig cells five times higher than in human endothelial cells was effective in inhibiting complement-dependent cytotoxicity of most human sera. However, 15- to 30-fold expression of hDAF was required for effective inhibition of human sera with the highest cytotoxic capacity. CONCLUSIONS: A much higher level of hDAF expression in pig cells than previously considered

DOI： 10.1111/j.1399-3089.2006.00365.x

PubMed

Effects of olprinone, a phosphodiesterase III inhibitor, on ischemic acute renal failure. 査読有り

Anas C, Ozaki T, Maruyama S, Yamamoto T, Gotoh M, Ono Y, Matsuo S

International journal of Urology 14 巻 ( 3 ) 頁： 219 - 225 2007年

Comparison of percutaneous coronary intervention with medication in the treatment of coronary artery disease in hemodialysis patients. 査読有り

Yasuda K, Kasuga H, Aoyama T, Takahashi H, Toriyama T, Kawade Y, Iwashima S, Yamada S, Kawahara H, Maruyama S, Yuzawa Y, Ishii H, Murohara T, Matsuo S

Journal of the American Society of Nephrology 17 巻 ( 8 ) 頁： 2322 - 2332 2006年8月

Geranylgeranylacetone ameliorates ischemic acute renal failure via induction of Hsp70. 査読有り

Suzuki S, Maruyama S, Sato W, Morita Y, Sato F, Miki Y, Kato S, Katsuno M, Sobue G, Yuzawa Y, Matsuo S

Kidney international 67 巻 ( 6 ) 頁： 2210 - 2220 2005年6月

Caveolin-1 in mesangial cells suppresses MAP kinase activation and cell proliferation induced by bFGF and PDGF. 査読有り

Fujita Y, Maruyama S, Kogo H, Matsuo S, Fujimoto T

Kidney international 66 巻 ( 5 ) 頁： 1794 - 1804 2004年11月

In vivo gene transfer of endo-beta-galactosidase C removes alphaGal antigen on erythrocytes and endothelial cells of the organs. 査読有り

Miki Y, Maruyama S, Liu D, Kobayashi T, Sato F, Shimizu H, Kato S, Sato W, Morita Y, Yuzawa Y, Muramatsu T, Matsuo S.

Xenotransplantation. 11 巻 ( 5 ) 頁： 444 - 451 2004年9月

記述言語：英語掲載種別：研究論文（学術雑誌）

BACKGROUND: The presence of Galalpha1-3Galbeta1-4GlcNAc (alphaGal) in pigs is a formidable barrier for pig-to-primate xenotransplantation. We have reported that administration of recombinant endo-beta-galactosidase C (EndoGalC) removes alphaGal on porcine erythrocytes and kidneys. The present study examined the effects of EndoGalC gene therapy on alphaGal suppression. METHODS: Naked plasmid DNA encoding Igkappa-EndoGalC was given to rats by rapid tail vein injection. The expression of alphaGal in the heart and kidney were studied by lectin staining followed by computer-assisted quantitative analyses. alphaGal expression on erythrocytes was determined by flow cytometric analyses. Enzymatic activity of EndoGalC in the serum was also determined by evaluating the capacity of EndoGalC in removing alphaGal epitopes. Elimination of alphaGal was further studied by injecting antibodies against alphaGal to rats 2 days after the gene transfer. RESULTS: Administration of 1 mg of Igkappa-EndoGalC/pCAGGS plasmid eliminated alphaGal from the vascular endothelium of the heart and kidney on day 1 and day 2. Between days 4 and 7, alphaGal started to reappear, but remained suppressed. No serious adverse effect was observed in rats treated with EndoGalC. Flow cytometric analyses showed that EndoGalC digested 97% of alphaGal on erythrocytes when measured 4 days after the gene transfer. Enzymatic activity of EndoGalC in the serum peaked on day 1, and significant levels were still observed on day 7. When antibodies against alphaGal were given, rats treated with EndoGalC showed no change, while all control rats died within 40 min. CONCLUSIONS: The present study demonstrates the potential of an EndoGalC gene transfer, using a hydrodynamics-based delivery system, in eliminating alphaGal from endothelial cells in vivo. The results also ensured that EndoGalC is not harmful suggesting that the production of pigs overexpressing EndoGalC would be a reasonable alternative to pigs deficient in alph

DOI： 10.1111/j.1399-3089.2004.00163.x

PubMed

Endotoxin-induced chemokine expression in murine peritoneal mesothelial cells: the role of toll-like receptor 4. 査読有り

Kato S, Yuzawa Y, Tsuboi N, Maruyama S, Morita Y, Matsuguchi T, Matsuo S.

J Am Soc Nephrol. 15 巻 ( 5 ) 頁： 1289 - 1299 2004年5月

記述言語：英語掲載種別：研究論文（学術雑誌）

Acute peritonitis, in which peritoneal mesothelial cells are directly exposed to bacterial components, is a major cause of peritoneal dysfunction in continuous ambulatory peritoneal dialysis patients. We have previously shown that Toll-like receptors (TLR) are expressed in kidney cells, and LPS induces TLR4-dependent chemokine production in tubular epithelial cells. The present work was designed to investigate the involvement of TLR, especially TLR4, in the lipid A-mediated chemokine production by murine peritoneal mesothelial cells (MPMC). A primary cell culture of MPMC from C3H/HeN mice (wild-type mice; LPS sensitive) and from C3H/HeJ mice (containing a point mutation of TLR4; LPS hyposensitive) was established. The expression profile of the TLR family and their accessory molecules, CD14 and MD-2, which are requisite for the LPS signaling pathway, was examined by RT-PCR, Northern blot test, and immunohistochemical staining. Synthetic lipid A-mediated chemokine production by MPMC was studied. The involvement of MAP kinase family (ERK, JNK, and p38 mitogen-activated protein kinase) and nuclear factor (NF)-kappaB in these processes was also studied. MPMC constitutively express TLR4, CD14, and MD-2. A prominent induction of monocyte chemotactic protein-1 (MCP-1) and macrophage inflammatory protein (MIP)-2 by MPMC was detected after lipid A stimulation and was strictly dependent on TLR4. Furthermore, TLR4-dependent chemokine production followed by leukocyte influx into the peritoneal cavity was also confirmed in vivo after stimulation with LPS. mRNA expression of MCP-1 was abolished by NF-kappaB inhibition, but were not affected by the inhibition of ERK, JNK, or p38. As compared with MCP-1, MIP-2 mRNA expression was inhibited by a high dose of curcumin but not by NF-kappaB decoy oligodeoxynucleotide and individual inhibitions of MAP kinase, suggesting that the additional signaling pathway with NF-kappaB might be involved in mRNA expression of MIP-2. These show that TLR

PubMed

The nephrotoxicity of Aristolochia manshuriensis in rats is attributable to its aristolochic acids. 査読有り

Liu MC, Maruyama S, Mizuno M, Morita Y, Hanaki S, Yuzawa Y, Matsuo S.

Clin Exp Nephrol. 7 巻 ( 3 ) 頁： 186 - 194 2003年9月

記述言語：英語掲載種別：研究論文（学術雑誌）

BACKGROUND: Although Aristolochia manshuriensis (AM), which was incriminated in the Japanese variety of Chinese herbs nephropathy, has been recently shown to be nephrotoxic in rats, less is known about whether this toxicity is attributable to its aristolochic acids (AA). We compared the renal effect of AM with that of Akebia quinata (AQ), which has similar components to AM but is free of AA; we also compared this effect of AM with that of pure AA, and studied its possible mechanism. METHODS: In study 1, rats were divided into four groups. Each group was orally given either 0.4 g of AM, 4 g of AM, or 4 g of AQ per day, or vehicle, for 5 days. In study 2, rats were given 4 g of AM (which contained 4 mg of AA), or 4 mg of pure AA per day, or vehicle, for 5 days. Renal function, and renal histology were evaluated on day 5 in study 1 and on days 1, 3, 5, and 14 in study 2. In study 2, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) and proliferating cell nuclear antigen (PCNA) staining were also performed. In study 3, rats were treated in the same way as in study 2, but were all killed on day 5. Concentrations of AA (I + II) were measured in serum and urine in study 2, and in the kidney, lung, heart, liver, and spleen in study 3. RESULTS: In study 1, only the rats that received 4 g/day of AM developed tubular necrosis, azotemia, proteinuria, and glucosuria. In study 2, both AM- and AA-treated rats showed progressive tubular damage, decreased renal function, and increased urinary protein excretion. The degree of these alterations was comparable in the AM and AA groups. Moreover, the concentrations of AA (I + II), in serum, urine, and kidney were also comparable in the AM- and AA-treated rats. High levels of AA were detected in the lung and kidney. Apoptotic tubular cells increased on day 5 and had decreased by day 14 after the withdrawal of AM or AA. Meanwhile, proliferating tubular cells progressively increased from day 3 to day 14. C

DOI： 10.1007/s10157-003-0229-z

PubMed

Non-dipping is a potent predictor of cardiovascular mortality and is associated with autonomic dysfunction in haemodialysis patients. 査読有り

Liu M, Takahashi H, Morita Y, Maruyama S, Mizuno M, Yuzawa Y, Watanabe M, Toriyama T, Kawahara H, Matsuo S.

Nephrol Dial Transplant. 18 巻 ( 3 ) 頁： 563 - 569 2003年5月

記述言語：英語掲載種別：研究論文（学術雑誌）

BACKGROUND: Lack of nocturnal blood pressure (BP) fall (non-dipping) is common among haemodialysis (HD) patients, but much less is known regarding its association with cardiovascular (CV) disease morbidity and mortality. METHODS: Eighty HD patients initially underwent 24 h ambulatory BP monitoring (ABPM), and then they were defined as either 'dippers' (n=24, nocturnal BP fall > or = 10%) or 'non-dippers' (n=56, fall <10%). Coronary angiography was performed in the patients who had signs and/or symptoms of coronary artery disease (CAD). Twenty-four hour ambulatory ECG was recorded in 20 dippers and 20 non-dipper HD patients, and in 20 normal subjects. All patients were followed for up to 5.8 years (33.0+/-19.1 months). The outcome events studied were the hospitalisations due to CV diseases and CV death. RESULTS: Compared with dippers, non-dippers initially had a higher incidence of coronary artery stenosis (P<0.05) along with left ventricular asynergy (both Ps<0.01). The circadian rhythm of autonomic function was impaired in non-dippers. The incidences of CV events and CV deaths were 3.5 and 9 times higher in non-dippers than in dippers. The cumulative CV event-free survival and CV survival rates were lower in non-dippers than in dippers (P=0.02 and P=0.005, respectively). Based on Cox analysis, non-dipping was associated positively with CV events and CV mortality [hazard ratio (HR) 2.46, 95% CI 1.02-5.92, P=0.038 and HR 9.62, 95% CI 1.23-75.42, P=0.031, respectively]. Meanwhile, nocturnal systolic BP fall, diurnal systolic BP and diurnal pulse pressure were negatively associated with CV event/death. The clinic BP was not associated with CV event/death. CONCLUSIONS: The non-dipping phenomenon is closely related to a high incidence of CV diseases, a poor long-term survival and profound autonomic dysfunction. ABPM is useful in predicting long-term CV prognosis in HD patients.

DOI： 10.1093/ndt/18.3.563

PubMed

Proteinuria and tubulointerstitial injury: the causative factors for the progression of renal diseases. 査読有り

Matsuo S, Morita Y, Maruyama S, Manchang L, Yuzawa Y.

Contrib Nephrol. 139 巻頁： 20 - 31 2003年

P-selectin-dependent macrophage migration into the tubulointerstitium in unilateral ureteral obstruction. 査読有り

Naruse T, Yuzawa Y, Akahori T, Mizuno M, Maruyama S, Kannagi R, Hotta N, Matsuo S.

Kidney Int. 62 巻 ( 1 ) 頁： 94 - 105 2002年7月

記述言語：英語掲載種別：研究論文（学術雑誌）

BACKGROUND: Interstitial infiltration of macrophages (Mø) is one of the main causal factors for the tubulointerstitial injury. However, precise mechanisms of Mø infiltration into tubulointerstitium have not been fully explored. The purposes of this study were to assess the role of selectins in the acute infiltration of Mø in rats with unilateral ureteral obstruction (UUO) and to evaluate the role of vasa recta, that is, whether they facilitate massive influx of Mø into the interstitium by functioning as specialized vessels. METHODS: To evaluate the role of selectins in Mø infiltration into tubulointerstitium, the expression of selectins and L-selectin ligands was examined by immunohistochemistry and immunoelectron microscopy. The functional role of P-selectin in vasa recta was studied by Stamper-Woodruff assay, in vivo p-Mø migration assay and in vivo blocking experiments with the monoclonal antibody (mAb) ARP2-4. RESULTS: Selective expression of P-selectin was detected in vasa recta as early as one hour after UUO, and the expression increased thereafter for 96 hours. In contrast, endothelial expression of L-selectin ligands and E-selectin were not detectable. In the Stamper-Woodruff assay on kidney sections of rats with UUO, the adhesion of isolated rat peritoneal Mø (p-Mø) to vasa recta was significantly inhibited by the mAb ARP2-4 (P-selectin blocker; P < 0.01), but not by mAb ARE-5 (E-selectin blocker) or rLECIg (rat L-selectin chimeric protein). In the in vivo transfer experiments with fluorescein-labeled p-Mø into rats 48 hours after UUO, labeled p-Mø had accumulated around vasa recta at three minutes and had infiltrated predominantly into the outer medulla at 180 minutes. The number of labeled p-Mø was reduced when the rats were pretreated with ARP2-4 (P < 0.01). Finally, ARP2-4 (10 mg/kg), injected 15 minutes before UUO, reduced the number of infiltrated Mø (P < 0.01). CONCLU

DOI： 10.1046/j.1523-1755.2002.00419.x

PubMed

Effects of human soluble thrombomodulin on experimental glomerulonephritis. 査読有り

Ikeguchi H, Maruyama S, Morita Y, Fujita Y, Kato T, Natori Y, Akatsu H, Campbell W, Okada N, Okada H, Yuzawa Y, Matsuo S.

Kidney Int. 61 巻 ( 2 ) 頁： 490 - 501 2002年2月

記述言語：英語掲載種別：研究論文（学術雑誌）

BACKGROUND: Coagulation and inflammation are both important processes that contribute to glomerular injury. The present study was performed to evaluate the effects of recombinant human soluble thrombomodulin (RHS-TM) in a lethal model of thrombotic glomerulonephritis and to investigate the possible mechanisms. METHODS: Thrombotic glomerulonephritis was induced in rats by administration of lipopolysaccharide and rabbit anti-rat glomerular basement membrane antibody. One hour later, RHS-TM or heparin was administered, and the histological findings, renal functions, and coagulation parameters were evaluated. To evaluate the contribution of carboxypeptidase R (CPR) to the results obtained in rats treated with RHS-TM, plasma CPR levels were measured. Then, carboxypeptidase inhibitor (CPI), which prevents the function of CPR, was administered. RESULTS: Massive glomerular thrombosis and lung hemorrhage developed within five hours of disease induction, and all rats died within 24 hours. RHS-TM (3 mg/kg) prevented the progression of the disease and all rats survived. Heparin (250 U/kg/h) showed similar anti-thrombotic effect, but induced massive hemorrhage in the lungs or stomach. RHS-TM attenuated leukocyte/neutrophil infiltration in the glomerulus but heparin did not, suggesting that RHS-TM has anti-inflammatory properties. CPR levels in plasma were about threefold higher in rats treated with RHS-TM compared to those in rats treated with heparin. Furthermore, the inhibitory effect of RHS-TM on leukocyte/neutrophil infiltration was significantly diminished by injection of CPI. CONCLUSION: RHS-TM effectively attenuates the injuries of thrombotic glomerulonephritis in rats. The results indicate that RHS-TM, in addition to its anti-thrombotic action, may exert its anti-inflammatory properties by converting proCPR to CPR, which then inactivates anaphylatoxins. RHS-TM is a potential novel therapeutic tool for thrombotic glomerular injury and related disorders.

DOI： 10.1046/j.1523-1755.2002.00160.x

PubMed

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