Faculty Profiles - MIZUNO, Masashi

Papers - MIZUNO, Masashi

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【特集:これだけは知っておきたい分子腎臓学2007】 C5a. Invited

水野正司、湯澤由紀夫、松尾清一

腎と透析 Vol. 63 page： 580-582 2007

Complement membrane attack is required for endplate damage and clinical disease in passive experimental myasthenia gravis in Lewis rats Reviewed International coauthorship International journal

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

CLINICAL AND EXPERIMENTAL IMMUNOLOGY Vol. 146 ( 2 ) page： 278 - 286 2006.11

Language：English Publishing type：Research paper (scientific journal) Publisher：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 Reviewed International coauthorship International journal

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

CLINICAL AND EXPERIMENTAL IMMUNOLOGY Vol. 146 ( 2 ) page： 294 - 302 2006.11

Language：English Publishing type：Research paper (scientific journal) Publisher：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 Vol. 69 ( 1 ) page： 23 - 34 2006.2

Complement and complement regulators in the male reproductive system Reviewed International coauthorship International journal

CL Harris, M Mizuno, BP Morgan

MOLECULAR IMMUNOLOGY Vol. 43 ( 1-2 ) page： 57 - 67 2006.1

Language：English Publishing type：Research paper (scientific journal) Publisher：PERGAMON-ELSEVIER SCIENCE LTD

Spermatozoa are almost unique among cells in that they must survive transplantation into a foreign host in order to perform their physiological role. The biggest hurdle to overcome is innate immune defence that will target the invaders in the female genital tract. Complement is a major player in innate immunity and is present in the female genital tract. Spermatozoa must therefore evade complement attack if they are to reach their goal. Complement evasion is achieved by the presence of complement regulators both in seminal plasma and on the spermatozoa. Here we discuss the parts played by complement and complement regulators in permitting spermatozoa to survive long enough to reach the oocyte, in clearance of the excess spermatozoa that have outlived their usefulness and in aiding activation of spermatozoa to engage the oocyte. In particular, we focus on the unique distribution patterns of complement regulators on spermatozoa, patterns that strongly suggest roles in spermatozoal development and oocyte binding. An understanding of these roles will inform studies of their contribution to fertility and infertility in man. (c) 2005 Elsevier Ltd. All rights reserved.

DOI： 10.1016/j.molimm.2005.06.026

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Stage-specific expression of CD55 isoforms during spermiogenesis in the rat

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

MOLECULAR IMMUNOLOGY Vol. 43 ( 1-2 ) page： 156 - 156 2006.1

The membrane attack pathway of complement drives pathology in experimental autoimmune myasthenia gravis in mice. Reviewed

Morgan BP., Chamberlain-Banoub J., Neal JW.,Song W., Mizuno M., Harris CL.

Clin Exp Immunol Vol. 146 page： 294-302 2006

Complement and complement regulators in the male reproductive system. Invited Reviewed

Harris CL., Mizuno M., Morgan BP.

Mol Immunol Vol. 43 page： 57-67 2006

Complement membrane attack is required for endplate damage and clinical disease in experimental myasthenia gravis in Lewis rats. Reviewed

Chamberlain-Banoub J., Neal JW., Mizuno M., Harris CL., Morgan BP.

Clin Exp Immunol Vol. 146 page： 278-286 2006

CD55 expression in rat male reproductive tissue: Differential expression in testis and expression of a unique truncated isoform on spermatozoa. Reviewed

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

Mol. Immunol. Vol. 44 page： 1624-1633 2006

A review of current knowledge of the complement system and the therapeutic opportunities in inflammatory arthritis. Invited Reviewed

Mizuno M.

Curr Med Chem Vol. 13 page： 1707-1717 2006

Unique expression patterns of membrane complement regulators and C3 in rat testes and spermatozoa delineate the blood-testis barrier and suggest distinct functional roles in germ cell development. Reviewed

Mizuno M., Harris CL., Morgan BP.

J Reprod Immunol Vol. 69 page： 23-34 2006

Mizuno M, Harris CL, Morgan BP

J Reprod Immunol Vol. 69 page： 23-34 2006

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

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

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