Faculty Profiles - MIZUNO, Masashi

Papers - MIZUNO, Masashi

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Shiga toxin 1causes direct renal injury in rats Reviewed International journal Open Access

Yamamoto ET, Mizuno M, Nishikawa K, Miyazawa S, Zhang LS, Matsuo S, Natori Y

INFECTION AND IMMUNITY Vol. 73 ( 11 ) page： 7099 - 7106 2005.11

Novel C5a regulators in inflammatory disease Invited Reviewed International journal

M Mizuno, DS Cole

EXPERT OPINION ON INVESTIGATIONAL DRUGS Vol. 14 ( 7 ) page： 807 - 821 2005.7

Authorship：Lead author,　Corresponding author Language：English Publishing type：Research paper (scientific journal) Publisher：ASHLEY PUBLICATIONS LTD

Complement is part of the innate immune system, acting to protect the host from microorganisms such as bacteria, and other foreign and abnormal cells. Although primarily protective, complement activation can also cause damage to the host. In a number of inflammatory diseases, including rheumatoid arthritis and dermatitis, there is excessive and inappropriate complement activation. Many of the toxic effects seen in these conditions are attributable to the excessive production of the anaphylatoxin C5a, which may contribute to both the initiation and progression of the disease. Therefore, the regulation of C5a production and modulation of its function are good pharmacological targets in these disorders. As yet, there are no effective agents for the therapeutic regulation of C5a in routine clinical practice. This review describes the role of C5a in inflammatory disease, animal models used to study C5a-related effects, and current strategies aimed at regulating C5a. There is also a discussion of the strengths and weaknesses of these approaches, and an outline of the likely progress of this class of drugs in the future.

DOI： 10.1517/13543784.14.7.807

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Expression of CD46 in developing rat spermatozoa: ultrastructural localisation and utility as a marker of the various stages of the seminiferous tubuli. Reviewed

Mizuno M., Harris CL., Suzuki N., Matsuo S., Morgan BP.

Biol Reprod Vol. 72 page： 908-915 2005

Shiga toxin-1 causes direct renal injury in rats. Reviewed

Yamamoto ET., Mizuno M., Nishikawa K., Miyazawa S., Zhang L., Matsuo S., Natori Y.

Infect Immun Vol. 73 page： 7099-7106 2005

Novel C5a regulators in inflammation. Invited Reviewed

Mizuno M., Cole DS.

Expert Opin Investig Drugs Vol. 14 page： 807-821 2005

CD59a is the primary regulator of membrane attack complex assembly in the mouse.

Baalasubramanian S, Harris CL, Donev RM, Mizuno M, Omidvar N, Song WC, Morgan BP

Journal of immunology (Baltimore, Md. : 1950) Vol. 173 ( 6 ) page： 3684 - 92 2004.9

Inummohistochemical analysis of membrane complement regulatory proteins in rat testis: unique roles for DAF and MCP in spermatozoal function?

Mizuno, M; Harris, CL; Morgan, BP

MOLECULAR IMMUNOLOGY Vol. 41 ( 2-3 ) page： 280 - 280 2004.6

The possibilities and pitfalls for anti-complement therapies in inflammatory diseases. Invited Reviewed

Mizuno M., Morgan BP.

Current Drug Targets Inflammation & Allergy Vol. 3 page： 85-94 2004

CD59a is the primary regulator of membrane attack complex assembly in the mouse. Reviewed

Baalasubramanian S., Harris CL., Donev RM., Mizuno M., Omidvar N., Song W., Morgan BP.

J. Immunol. Vol. 173 page： 3684-3692 2004

Rat membrane cofactor protein (MCP; CD46) is expressed only in the acrosome of developing and mature spermatozoa and mediates binding to immobilized activated C3. Reviewed

Mizuno M., Harris CL., Johnson PM., Morgan BP.

Biol Reprod Vol. 71 page： 1374-1383 2004

Deletion of the gene encoding CD59a in mice increases disease severity in a murine model of rheumatoid arthritis. Reviewed

Williams AS., Mizuno M., Richards PJ., Holt DS., Morgan BP

Arthritis Rheum Vol. 50 page： 3035-3044 2004

In two patients on long-term hemodialysis, Etidronate Disodium improved their discomfort and extremities' blood flow associated with severe abnormal arterial wall calcification. Reviewed

Mizuno M., Kashima N., Kato K., Ito A, Matsuo S.

Clin Drug Invest Vol. 24 page： 365-371 2004

Improvement in Discomfort and Decreased Blood Flow Associated with Severe Arterial Wall Calcification following Etidronic Acid. Reviewed International journal

Mizuno M, Kashima N, Kato K, Ito A, Matsuo S

Clinical drug investigation Vol. 24 ( 6 ) page： 365 - 71 2004

Implication of the complement system in the induction of antiglomerular basement membrane glomerulonephritis in WKY rats Reviewed International journal

SHIKE Tatsuhiko, ISOME Masato, MIZUNO Masashi, SUZUKI Junzo, MATSUO Seiichi, YAMAMOTO Tadashi, SUZUKI Hitoshi

Pathol Int Vol. 53 ( 11 ) page： 757 - 761 2003.11

Implication of the complement system in the induction of anti-glomerular basement membrane glomerulonephritis in WKY rats.

Shike T, Isome M, Mizuno M, Suzuki J, Matsuo S, Yamamoto T, Suzuki H

Pathology international Vol. 53 ( 11 ) page： 757 - 61 2003.11

The nephrotoxicity of Aristolochia manshuriensis in rats is attributable to its aristolochic acids

LIU Man-Chang, MARUYAMA Shoichi, MIZUNO Masashi, MORITA Yoshiki, HANAKI Shigeru, YUZAWA Yukio, MATSUO Seiichi

Clinical and experimental nephrology Vol. 7 ( 3 ) page： 186 - 194 2003.9

The nephrotoxicity of Aristolochia manshuriensis in rats is attributable to its aristolochic acids Reviewed International journal

Man-Chang Liu, Shoichi Maruyama, Masashi Mizuno, Yoshiki Morita, Shigeru Hanaki, Yukio Yuzawa, Seiichi Matsuo

Clinical and Experimental Nephrology Vol. 7 ( 3 ) page： 186 - 194 2003.9

Language：English Publishing type：Research paper (scientific journal)

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. Conclusions. Our study indicates that the renal toxicity of AM can be attributed to its AA component. Tubular cell apoptosis might be one of the mechanisms involved in this renal injury.

DOI： 10.1007/s10157-003-0229-z

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Membrane cofactor protein (MCP; CD46) in the rat is expressed only in male germ cells and precursors

Mizuno, M; Harris, CL; Morgan, BP

MOLECULAR IMMUNOLOGY Vol. 40 ( 2-4 ) page： 202 - 203 2003.9

Characterization of the mouse analogues of CD59 using novel monoclonal antibodies: tissue distribution and functional comparison.

Harris CL, Hanna SM, Mizuno M, Holt DS, Marchbank KJ, Morgan BP

Immunology Vol. 109 ( 1 ) page： 117 - 26 2003.5

Characterization of the mouse analogues of CD59 using novel monoclonal antibodies: tissue distribution and functional comparison Reviewed International coauthorship International journal

CL Harris, SM Hanna, M Mizuno, DS Holt, KJ Marchbank, BP Morgan

IMMUNOLOGY Vol. 109 ( 1 ) page： 117 - 126 2003.5

Language：English Publishing type：Research paper (scientific journal) Publisher：BLACKWELL PUBLISHING LTD

CD59, the sole membrane regulator of the membrane attack complex of complement, is broadly and abundantly expressed in man and other mammals. In mouse, CD59 is encoded by two homologous genes. The expression patterns and functional roles of the proteins encoded by these genes, mCD59a and mCD59b, have not been well characterized. Here we describe the generation of monoclonal and polyclonal antibodies detecting specifically mCD59a and mCD59b. These reagents have been used to study function and to ascertain the cell and tissue distributions of mCD59a and mCD59b. mCD59a was broadly distributed on endothelia, erythrocytes, platelets, and on numerous other cell types in organs, a distribution pattern resembling that of CD59 in other species. In marked contrast, expression of mCD59b was restricted to germ cell elements in the testis and mature spermatozoa. Both mCD59a and CD59b inhibited human and rodent complement with similar efficiency. These findings demonstrate that the broadly distributed mCD59a is the key regulator of the terminal complement pathway in mice whereas CD59b, expressed only in testis and on sperm, probably plays other roles in vivo.

DOI： 10.1046/j.1365-2567.2003.01628.x

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