研究者詳細 - 水野　正司

論文 - 水野　正司

分割表示 334 件中 221 - 240 件目／全件表示 >>

The mouse complement regulator CD59b is significantly expressed only in testis and plays roles in sperm acrosome activation and motility. 査読有り

Donev RM., Sivasankar B., Mizuno M., Morgan BP.

Mol. Immunol. 45 巻頁： 534-542 2008年1月

The mouse complement regulator CD59b is significantly expressed only in testis and plays roles in sperm acrosome activation and motility. 査読有り国際共著国際誌

Donev RM, Sivasankar B, Mizuno M, Morgan BP

Molecular immunology 45 巻 ( 2 ) 頁： 534 - 542 2008年1月

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.

Am J Physiol Renal Physiol 294 巻頁： F1084-F1093 2008年

『特集　アシドーシスとアルカローシス』代謝性酸塩基平衡異常における治療の基本とその方法招待有り

伊藤恭彦、水野正司

薬局 59 巻頁： 42-47 2008年

本邦のCAPD療法の現況　–　CAPD療法に対する取り組み　大学・教育病院の役割招待有り

伊藤恭彦、水野正司、丸山彰一、湯澤　由紀夫、松尾清一

臨床透析 24 巻頁： 205-210 2008年

Complement C3a receptor was highly found in the glomeruli of inflamed human lupus nephritis 国際共著国際誌

Mizuno, M; Blanchin, S; Gasque, P; Nishikawa, K; Matsuo, S

MOLECULAR IMMUNOLOGY 44 巻 ( 16 ) 頁： 3953 - 3953 2007年9月

CD59b is abundantly expressed only in testis and plays a role in acrosome activation and spermatozoal motility 査読有り国際共著国際誌

Donev, RM; Sivasankar, B; Mizuno, M; Morgan, BP

MOLECULAR IMMUNOLOGY 44 巻 ( 16 ) 頁： 3956 - 3956 2007年9月

A protein toxin from the sea anemone Phyllodiscus semoni targets the kidney and causes a renal injury resembling haemolytic uremic syndrome. 査読有り

Mizuno M., Nozaki M., Morine N., Suzuki N., Nishikawa K., Morgan BP., Matsuo S.

Am. J. Pathol. 171 巻頁： 402-414 2007年8月

担当区分：筆頭著者記述言語：英語掲載種別：研究論文（学術雑誌）

Envenomation by the sea anemone Phyllodiscus semoni causes fulminant dermatitis and, rarely, acute renal failure in humans. Here, we investigated whether the venom extracted from the nematocysts (PsTX-T) was nephrotoxic when administered intravenously in rats and whether PsTX-T induced activation of the complement system. Although small dose of PsTX-T induced acute tubular necrosis in rats resembling pathology seen in patients, kidneys displayed glomerular injury with glomerular endothelial damage, thrombus formation, mesangiolysis, and partial rupture of glomerular basement membrane, accompanied by severe tubular necrosis at 24 hours after administration of 0.03 mg of PsTX-T per animal, similar to the glomerular findings typical of severe hemolytic uremic syndrome. The early stage injury was accompanied by specific PsTX-T binding, massive complement C3b, and membrane attack complex deposition in glomeruli in the regions of injury and decreased glomerular expression of complement regulators. A pathogenic role for complement was confirmed by demonstrating that systemic complement inhibition reduced renal injury. The isolated nephrotoxic component, a 115-kd protein toxin (PsTX-115), was shown to cause identical renal pathology. The demonstration that PsTX-T and PsTX-115 were highly nephrotoxic acting via induction of complement activation suggests that inhibition of complement might be used to prevent acute renal damage following envenomation by P. semoni.

CD55 in rat male reproductive tissue: Differential expression in testis and expression of a unique truncated isoform on spermatozoa 国際共著国際誌

Mizuno, M; Donev, RM; Harris, CL; Morgan, BP

MOLECULAR IMMUNOLOGY 44 巻 ( 7 ) 頁： 1613 - 1622 2007年3月

Immunisation with CD46 generates a strong autoantibody response targeting the spermatozoal acrosome in rat

Mizuno, M; Harris, CL; Morgan, BP

MOLECULAR IMMUNOLOGY 44 巻 ( 1-3 ) 頁： 216 - 216 2007年1月

High levels of complement C3a receptor in the glomeruli of inflamed human lupus nephritis. 査読有り

Mizuno M., Blanchin S., Gasque P., Nishikawa K., Matsuo S.

Am. J. Kidney Dis. 49 巻頁： 598-606 2007年

担当区分：筆頭著者記述言語：英語掲載種別：研究論文（学術雑誌）

BACKGROUND: Taking into consideration the key role of the complement system in renal diseases, we investigated molecular and cellular properties of the human complement C3a receptor (C3aR) in vitro and in situ, looking at its expression in several human renal pathological states. METHODS: Several antibodies were generated and used for immunohistochemistry and Western blot analyses to address C3aR expression and its regulation in vitro on cell lines of myeloid cells and nonmyeloid cell lineages. Furthermore, C3aR distribution was investigated in control nephrectomized kidneys and 116 biopsy specimens from patients with renal diseases, including lupus nephritis (lupus-N). RESULTS: C3aR is a highly N-glycosylated protein with an apparent molecular mass of 65 to 95 kd expressed by myeloid and endothelial cells. C3aR is particularly upregulated in response to interferon gamma treatment, but was unaffected by the other inflammatory cytokines, such as tumor necrosis factor alpha and transforming growth factor beta. In normal human kidney, C3aR staining was not observed. However, glomerular C3aR staining was detected in 42.9% of lupus-N specimens in association with immunoglobulin G immune-complex depositions. Staining intensity correlated with disease severity. C3aR was found in the endothelial area of 81.3% of samples classified as World Health Organization class IV with active lesions. Conversely, C3aR was not detected by means of immunohistochemistry in kidneys from patients with other renal diseases. CONCLUSION: Our data indicate that C3aR expression is tightly regulated and altered in certain disease conditions. C3aR may be used as a unique biomarker of diagnosis and disease activity in patients with lupus-N.

よく使う利尿薬について習熟する　スピロノラクトン招待有り

水野正司、伊藤恭彦

Medicina 44 巻頁： 359-342 2007年

Immunization with autologous CD46 in rats generates a strong autoantibody response that targets spermatozoa. 査読有り

Mizuno M., Harris CL., Morgan BP.

J. Reprod. Immunol. 73 巻頁： 135-147 2007年

【特集:これだけは知っておきたい分子腎臓学2007】 C5a. 招待有り

水野正司、湯澤由紀夫、松尾清一

腎と透析 63 巻頁： 580-582 2007年

Complement membrane attack is required for endplate damage and clinical disease in passive experimental myasthenia gravis in Lewis rats 査読有り国際共著国際誌

J. Chamberlain-Banoub, J. W. Neal, M. Mizuno, C. L. Harris, B. P. Morgan

CLINICAL AND EXPERIMENTAL IMMUNOLOGY 146 巻 ( 2 ) 頁： 278 - 286 2006年11月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：BLACKWELL PUBLISHING

Myasthenia gravis (MG) is a debilitating and potentially fatal neuromuscular disease characterized by the generation of autoantibodies reactive with nicotinic acetylcholine receptors (AChR) that cause loss of AChR from the neuromuscular endplate with resultant failure of neuromuscular transmission. A role for complement (C) in the pathology of human MG has been suggested based upon identification of C activation products in plasma and deposited at the endplate in MG. In the rat model, experimental autoimmune MG (EAMG), C depletion or inhibition restricts clinical disease, further implicating C in pathology. The mechanisms by which C activation drives pathology in MG and EAMG are unclear. Here we provide further evidence implicating C and specifically the membrane attack complex (MAC) in the Lewis rat passive EAMG model of MG. Rats deficient in C6, an essential component of the MAC, were resistant to disease induction and endplate destruction was reduced markedly compared to C6-sufficient controls. After reconstitution with C6, disease severity and endplate destruction in the C6-deficient rats was equivalent to that in controls. The data confirm the essential role of the MAC in the destruction of the endplate in EAMG and raise the prospect of specific MAC inhibition as an alternative therapy in MG patients resistant to conventional treatments.

DOI： 10.1111/j.1365-2249.2006.03198.x

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The membrane attack pathway of complement drives pathology in passively induced experimental autoimmune myasthenia gravis in mice 査読有り国際共著国際誌

B. P. Morgan, J. Chamberlain-Banoub, J. W. Neal, W. Song, M. Mizuno, C. L. Harris

CLINICAL AND EXPERIMENTAL IMMUNOLOGY 146 巻 ( 2 ) 頁： 294 - 302 2006年11月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：BLACKWELL PUBLISHING

The human neuromuscular disease myasthenia gravis (MG) is characterized by the generation of autoantibodies reactive with nicotinic acetylcholine receptors (AChR) that cause loss of AChR from the neuromuscular end-plate with resultant failure of neuromuscular transmission. A role for complement (C) in AChR loss has been suggested based uponmorphological identification of C at the end-plate in MG and from the effects of C inhibition in murine models. Here we provide further evidence implicating C, and specifically the membrane attack complex (MAC), in a mouse model of MG. Mice deficient in the C regulators Daf1 and/or Cd59a were tested in the model. Wild-type mice were resistant to disease while mice deficient in Daf1 had mild disease symptoms with evidence of C activation and AChR loss at end-plates. Cd59a-deficient mice had very mild disease with some muscle inflammation and essentially undamaged end-plates. In contrast, mice deficient in both C regulators developed a severe paralytic disease with marked muscle inflammation and loss of end-plates. Inhibition of MAC assembly abrogated clinical disease in these double-deficient mice, demonstrating conclusively that MAC formation was driving pathology in the model. These findings provoke us to suggest that current anti-C therapeutics targeting MAC assembly will be beneficial in MG patients resistant to conventional therapies.

DOI： 10.1111/j.1365-2249.2006.03205.x

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Spermatogenic cells distal to the blood-testis barrier in rats lack C3 convertase regulators and may be at risk of complement-mediated injury.

Mizuno M, Harris CL, Morgan BP

Journal of reproductive immunology 69 巻 ( 1 ) 頁： 23 - 34 2006年2月