Juntendo University, Tokyo, established in 1838.

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  4. Iwao Sekigawa, MD, PhD.

Institute for Environmental and Gender-Specific Medicine

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Iwao Sekigawa, MD, PhD.

MD: Fukushima Medical University (1978)
PhD: Juntendo University School of Medicine (1987)

Education and Appointments:

1978 Graduation from Fukushima Medical College (M.D.)
1985-1988 Juntendo University Faculty of Medicine,
Department of Pathology,
Instructor (Ph.D.)
1988-1991 Harvard Medical School, New England Deaconess Hospital
Department Hematology/Oncology,
Instructor
1991-1995 Juntendo University Faculty of Medicine,
Department of Internal Medicine and Rheumatology, Instructor
1995-2004 Juntendo University Faculty of Medicine,
Department of Internal Medicine and Rheumatology,
Assistant professor
2004-2008 Juntendo University Faculty of Medicine,
Department of Internal Medicine and Rheumatology,
Associate professor
Juntendo University Graduate School of Medicine,
The Institute for Environment and Gender-Specific Medicine,
Associate professor (concurrent)
2008- Juntendo University Faculty of Medicine,
Department of Internal Medicine and Rheumatology,
Professor
Juntendo University Graduate School of Medicine,
The Institute for Environment and Gender-Specific Medicine,
Professor (concurrent)

Members:

Hiroshi Kaneko MD, PhD.
Hitoshi Ogasawara MD, PhD.
Kazuhisa Nozawa MD, PhD.Assistant Professor
Keigo Ikeda MD, PhD. Assistant Professor
Mikiko Kawasaki PhD. Postdoctral Fellow
Ayako Yamaguchi MD. Graduate Student
Maki Fujishiro. Research Assistant

Research Specialty:

   The incidence of certain autoimmune diseases such as systemic lupus erythematosus (SLE) is well known to be far higher in females than in males.  We are interested in the gender bias of autoimmune diseases, especially (SLE), and mainly investigating the mechanisms of such sexual differences.

Research description:

1) The pathogenesis of SLE: We have been investigating the possible role of human endogenous retroviruses (HERV) on the induction of SLE, and reported the higher transcription and translation of HERV in SLE patients as compared to controls. We examine the mechanisms (especially epigenetic regulation, including DNA methylation and acethylation) of increased transcription of HERV in the patients with SLE.

2) With reference to 1), we also investigate the fluctuation of gene expressions in SLE patients along with the disease activities using a DNA micro array method. The effect of sex hormones on gene expressions are also examined by using the same method. Furthermore, in order to make clear the mechanisms of gender bias of SLE, we are performing the quantitative and qualitative analyses of hormone (such as estrogen-alpha and beta) receptors in the patients with SLE.

3) Clinical studies relating to autoimmune diseases are also performed. For instance, we are investigating the relationship between fetal loss of mothers having with autoimmune diseases and certain autoantibodies, and the precise mechanisms of the therapeutic effect of anti-tumor necrosis factor (TNF)-alpha antibodies, which is a most recent treatment to rheumatoid arthritis (RA), on the patients with RA.
   In addition, through the case studies of patients with autoimmune and/or rheumatic diseases, we also explore the establishment of new clinical features or entities, as well as more effective therapeutic approaches for these disorders.
   These studies seem to contribute to the elucidation of the pathogenesis of SLE or RA as well as the mechanisms of gender bias of these disorders, and the development of new treatments of them.

Research contents:

  We are investigating the pathogenesis of autoimmune diseases including rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) using modern biological technologies such as mass spectrometry and DNA/RNA microarrays, and seeking new diagnostic/therapeutic approaches from data obtained in our research.

1) Rheumatoid arthritis (RA): We are investigating the mechanisms underlying the efficacy of recently developed biological drugs for RA (including infliximab, etanercept, adalimumab and tocilizmab) using mass spectrometry. We have found that certain serum/plasma proteins show remarkable quantitative changes in RA patients before and after treatment. We are developing new therapeutic strategies and diagnostic technologies targeting these proteins, using RA model mice and human RA samples.

2) Systemic lupus erythematosus (SLE): We are investigating SLE-disease-activity-related genes in peripheral blood mononuclear cells (PBMC) from SLE patients using DNA microarray methods. Our data have suggested an important role of interferon regulatory genes (IFRg) in the activation of SLE. Furthermore, we found abnormal activities of IFRg-related gene cascades in SLE patients by using pathway network analysis. We have examined the therapeutic efficacy of a drug which has inhibitory effects on these gene cascades in model mice of SLE.

3) Mechanisms of gender bias in incidence of autoimmune diseases such as SLE, RA, and Sjogren’s syndrome (SS) are also investigated in our laboratory. In addition, the role of microRNA in the translation/transcription of genes in RA and/or SLE are studied using the latest microRNA analysis technology.

Publications (2005-2012)

  1. Fujishiro M, Nozawa K, Kawasaki M, Yamaguchi A, Iwabuchi K, Yanagida M, Suzuki F, Miyazawa K, Fukui H, Kaneko K, Ogawa H, Takamori K, Takasaki Y, Sekigawa I. Regenerating gene (REG) 1 alpha promotes pannus progression in patients with rheumatoid arthritis. Mod Rheumatol 22, 228-237, 2012
  2. Fujishiro M, Yamaguchi A, Kawasaki M, Nozawa K, Takasaki Y, Takamori K, Ogawa H, Endo K, Ng PS, Takehara K, Sekigawa I. The detection of plasma levels of connective tissue growth factor in rheumatoid arthritis patients. Clin Exp Rheumatol 30, 145-146, 2012
  3. Yamaguchi A, Nozawa K, Fujishiro M, Kawasaki M, Takamori K, Ogawa H, Sekigawa I, Takasaki Y. Estrogen inhibits apoptosis and promotes CC motif chemokine ligand 13 expression on synovial fibroblasts in rheumatoid arthritis. Immunopharmacol Immunotoxicol. 2012 Mar 7 [Epub ahead of print]
  4. Kimura U, Kinoshita A, Sekigawa I, Takamori K, Suga Y. Successful treatment with adalimumab in a patient with psoriatic arthritis and generalized pustular psoriasis. J Dermatol. 2012 Apr 16. doi: 10.1111/j.1346-8138.2012.01563.x. [Epub ahead of print]
  5. Nozawa K, Fujishiro M, Takasaki Y, Takamori K, Ogawa H, Sekigawa I: Mechanism of disease amelioration on infliximab treatment: novel effecter molecules for pathogenesis of rheumatoid arthritis. Infliximab, 168-176, 2012, Nova Science Publishers Inc., New York.
  6. Kawasaki M, Fujishiro M, Yamaguchi A, Nozawa K, Kaneko H, Takasaki Y, Takamori K, Ogawa H, Sekigawa I: Possible role of the JAK/STAT pathways in the regulation of T cell-interferon related genes in systemic lupus erythematosus. Lupus 20, 1231-1239, 2011
  7. Yamada R, Nozawa K, Yoshimine T, Takasaki Y, Ogawa H, Takamori K, Sekigawa I. A Case of Thrombotic Thrombocytopenia Purpura Associated with Systemic Lupus Erythematosus: Diagnostic Utility of ADAMTS-13 Activity. Autoimmune Dis. 2011;2011:483642. Epub 2011 Jul 11.
  8. Kawasaki M, Fujishiro M, Yamaguchi A, Nozawa K, Kaneko H, Takasaki Y, Takamori K, Ogawa H, Sekigawa I: Fluctuations in the gene expression of peripheral blood mononuclear cells between the active and inactive phases of systemic lupus erythematosus. Clin Exp Rheumatol 28, 311-317, 2010.
  9. Nozawa K, Fujisiro M, Kawasaki M, Kaneko H, Iwabuchi K, Yanagida M, Suzuki F, Miyazawa K, Takasaki Y, Ogawa H, Takamori K, Sekigawa I: Connective tissue growth factor promotes articular damage by increased osteoclastogenesis in patients with rheumatoid arthritis: novel protective mechanism of articular destruction on anti-TNF-alpha blocking therapy. Arthritis Res Ther 11, R174, 2009.
  10. Nozawa K, Kaneko H, Itoh T, Katsura Y, Noguchi M, Suzuki F, Takasaki Y, Ogawa H, Takamori K, Sekigawa I: Synchronous malignant B-cell lymphomanand gastric tubular adenocarcinoma associated with paraneoplastic cutaneous vasculitis: hypereosinophilic syndrome with mixed cryoglobulinemia is an important sigh of paraneoplastic syndrome. Rare Tumors 1, 54-57, 2009.
  11. Kawasaki M, Sekigawa I, Nozawa K, Kaneko H, Takasaki Y, Takamori K, Ogawa H: Changes in the gene expression of peripheral blood mononuclear cells during the menstrual cycle of females is associated with a gender bias in the incidence of systemic lupus erythematosus. Clin Exp Rheumatol 27, 260-266, 2009.
  12. Nozawa K, Ikeda K, Sato M, Reeves WH, Stewart CM, Li YC, Yen TJ, Rios RM, Takamori K, Ogawa H, Sekigawa I, Takasaki Y, Chan EKL: Autoantibody to nuclear antigen NA14 is an independent marker primarily for Sjogren’s syndrome. Front Biosci 14, 3733-3739, 2009.
  13. Sekigawa I, Fujishiro F, Yamaguchi A, Kawasaki M, Inui A, Nozawa K, Takasaki Y, Takamori K, Ogawa H: A new hypothesis of the possible mechanisms of gender differences in systemic lupus erythematosus. Clin Exp Rheumatol 28, 419-423, 2009.
  14. Morimoto K, Tokano Y, Nakano S, Watanabe T, Tamayama Y, Mitsuo A, Suzuki J, Kaneko H, Sekigawa I, Takasaki Y: Chemoattractant mechanism of Th1 cells in class III and IV lupus nephritis. Autoimmunity 42, 143-149, 2009.
  15. Sekigawa I, Kaneda K, Kaneko H, Takasaki Y, Takamori K, Ogawa H: Detection of serum IgE class anti-SSA antibodies in mothers with foetal loss. Rheumatol Int 28, 623-626, 2008.
  16. Sekigawa I, Yanagida M, Iwabuchi K, Kaneda K, Kaneko H, Takasaki Y, Jung G, Sone S, Tanaka Y, Ogawa H, Takamori K: Protein biomarker analysis by mass spectrometry in patients with rheumatoid arthritis receiving anti-tumor necrosis factor-α antibody therapy. Clin Exp Rheumatol 26, 261-267, 2008.
  17. Kawasaki M, Kaneda K, Kaneko H, Sekigawa I, Takasaki Y, Ogawa H: Two cases of dermatomyositis associated with interstitial pneumonia: Comprehensive study of gene expression. Clin Exp Rheumatol 26, 379-380, 2008.
  18. Naito T, Inui A, Kudo N, Matsumoto N, Fukuda H, Isonuma H, Sekigawa I, Dambara T, Hayashida Y: Seroprevalence of IgG anti-Toxoplasma antibodies in asymptomatic patients infected with human immunodeficiency virus in Japan. Intern Med, 2007; 46: 1149-1150.
  19. Inui A, Ogasawara H, Naito T, Sekigawa I, Takasaki Y, Hayashida Y, Takamori K, Ogawa H: Estrogen receptor expression by peripheral blood mononuclear cells of patients with systemic lupus erythematosus. Clin Rheumatol,2007; 26: 1675-1678.
  20. Sekigawa I, Kawasaki M, Ogasawara H, Kaneko H, Takasaki Y, Hashimoto H, Ogawa H: Possible role of DNA methylation in the induction of systemic lupus erythematosus. Current Rheumatology Reviews, 2007: 3: 11-16.
  21. Sekigawa I, Kawasaki M, Ogasawara H, Kaneda K, Kaneko H, Takasaki Y, Ogawa H: DNA methylation: its contribution to systemic lupus erythematosus. Clin Exp Med, 2006; 6: 99-106.
  22. Nakamura T, Sekigawa I, Ogasawara H, Mitsuishi K, Hira K, Ikeda S, Ogawa H: Expression of DNMT-1 in patients with atopic dermatitis. Arch Dermal Res, 2006;298: 253-256.
  23. Yamamoto N, Tanaka C, Wu Y, Chang MO, Inagaki Y, Sato Y, Naito T, Ogasawara H, Sekigawa I, Hayashida Y: Analysis of human immunodeficiency virus type 1 integration by using a specific, sensitive and quantitative assay based on real-time polymerase chain reaction. Virus genes, 2006; 32: 105-113.
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