Juntendo University, Tokyo, established in 1838.

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  4. Kenji Takamori MD, Ph.D

Institute for Environmental and Gender-Specific Medicine

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Kenji Takamori MD, Ph.D

  • Professor, Department of Dermatology, Juntendo University School of Medicine
  • Director of Juntendo University Urayasu Hospital
  • Professor and Chairman, Institute for Environmental and Gender-specific
    Medicine, Juntendo University Graduate School of Medicine

Research group members:

Mitsutoshi Tominaga PhD.  Postdoctral fellow
Sumiko Ozawa  Graduate student (Department of Dermatology, Juntendo University Urayasu hospital)

Research Speciality:

We will focus on glycosphingolipid-supramolecular domains-mediated functions in innate immunity.

Research Description:

※ Mechanisms of intraepidermal neurite formation in dry skin
※ Peripheral opiate receptor system in human epidermis and itch
※ Development of new drugs for pruritic disease
※ Proteomics analysis of allergic disease and autoimmune bullous disease

Research interest:

Pruritus is a common symptom in various dermatological disorders such as xerosis and atopic dermatitis (AD), which are characterized by dry skin. Our previous studies revealed that many nerve fibers existed in epidermis of xerosis and AD, raising the possibility that neuritogenesis in epidermis is related to itching in the skin. However, the mechanisms of intraepidermal neurite formation are poorly understood. We analyzed the neurite formation mechanisms using dry skin model mice, which are treated with acetone solution for cutaneous barrier disruption, and NC/Nga mice as an AD model. PGP9.5-positive nerve fibers were observed abundantly in epidermis of both the models. Levels of NGF and gelatinase activity were increased in the epidermis of these model mice. These results suggest that NGF promotes the growth of nerve fibers in epidermis, and gelatinase released from keratinocytes gives the spaces in among keratinocytes for neurite formation.

Pruritus is one of the most common side effects of epidurally or intrathecally administered morphine (a μ-opioid receptor agonist) in human. This effect is thought to be caused by the μ-opioid receptor. Furthermore, the μ-opioid antagonists naloxone and naltrexone have been reported to suppress pruritus in patients with chronic cholestasis, chronic renal failure, and AD. These observations suggest that the μ-opioid system is involved in itching. In contrast, there are few data about the involvement of other opioid receptors in itching. Recently, we found a novel κ-opioid agonist, TRK-820, and demonstrated that TRK-820 had efficacy against antihistamine-resistant pruritus via κ-opioid receptors. It has been reported that human epidermal keratinocytes expressed μ-opioid receptors not only in mRNA but also protein levels. Therefore, we are currently focusing on analyzing the involvement of peripheral opiate receptor system in itching in the skin.

Reference (selected)

  1. Yamakura F, Matsumoto T, Ikeda K, Taka H, Fujimura T, Murayama K, Watanabe E, Tamaki M, Imai T, Takamori K. Nitrated and oxidized products of a single tryptophan residue in human Cu,Zn-superoxide dismutase treated with either peroxynitrite-carbon dioxide or myeloperoxidase-hydrogen peroxide-nitrite. J Biochem (Tokyo). 138: 57-69, 2005
  2. Inagaki T, Suzuki T, Shimizu H, Ishii N, UmezawaY, Tada J, Kikuchi N, Takata M, Takamori K, Kishibe , Tanaka M, Miyamura Y, Tomita Y. Oculocutaneous albinism Type 4 is one of the most common types of Albinism in Japan. Am.J.Hum. Genet. 74: 466-471, 2004
  3. Murayama N, Takimoto R, Kawai M, Hiruma M, Takamori K, Nishimura K. A case of subcutaneous phaeohyphomycotic cyst due to Exophiala jeanselmei complicated with systemic lupus erythematosus. Mycoses. 46: 145-8, 2003
  4. Matsuba S, Suga Y, Ishidoh K, Hashimoto Y, Takamori K, Kominami E, Wilhelm B, Seitz J, Ogawa H. Sulfhydryl oxidase (SOx) from mouse epidermis: molecular cloning, nucleotide sequence, and expression of recombinant protein in the cultured cells. J Dermatol Sci. 30: 50-62, 2002
  5. Palingwachira P, Kakuta M, Yamazaki M, Yaguchi H, Tsuboi R, Takamori K, Ogawa H. Immunohistochemical localization of Cathepsin L and A in normalskin and skin tumors. J.Dermatol. 29: 573-579, 2002
  6. Takamori K. Recent advances in the treatment of autoimmune bullous diseases. J Dermatol. 28: 654-7, 2001
  7. Kawada A, Gomi H, Shiraishi H, Hatanaka K, Matsuo I, Inahuku K, Takamori K, Tezuka T, An infantile case of erythropoietic protoporphylia with a decreased RNA level of ferrochelatase. Hihu 43: 111-115, 2001
  8. Hashimoto Y, Suga Y, Matsuba S, Mizoguchi M, Takamori K, Seitz J, Ogawa H, Inquiry into the role of skin sulfhydryl oxidase (SOx) in epidermal disulfide bond formation-Implication of the localization and regulation of skin SOx as revealed by TPA, retinoic acid, and UVB radiation. J. Invest. Dermatol. 117: 752-754, 2001
  9. Palungwachira P, Chirachanakul P, Chalugun P, Nakao A, Takamori K, Ogawa H. Cutaneous findings in HIV-1 positive patients in Thailand. J. Dermatol., 28: 584-585, 2001
  10. Takamori K. Recent advances in the treatment of autoimmune bullous diseases. J. Dermatol. 28: 654-657, 2001
  11. Suto H, Mitsuishi K, Hira K, Uchida T, Unno T, Ogawa H, Yoshiike T, Takamori K. [The effect of suplatast tosilate on immunological parameters for the patients with atopic dermatitis] Arerugi. 49: 1163-72, 2000
  12. Hashimoto Y, Suga Y, Matsuba S, Mizoguchi M, Takamori K, Seitz J, Ogawa H. Immunohistochemical localization of sulfhydryl oxidase correlates with disulfide crosslinking in the upper epidermis of rat skin. Arch Dermatol Res. 292: 570-2, 2000
  13. Yamazaki M, Kakuta M, Takimoto R, Murayama N, Takamori K. Nasal natural killer cell lymphoma presenting as lethal midline granuloma. Int J Dermatol. 39: 931-4, 2000
  14. Hashimoto Y, Suga Y, Yoshiike T, Hashimoto T, Takamori K. A case of antiepiligrin cicatricial pemphigoid successfully treated by plasmapheresis. Dermatology 201: 58-60, 2000
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