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My dissertation

Inkin Ujiie

Altered balance of epidermis-related chemokines in epidermolysis bullosa.
J Dermatol Sci 86: 37-45, 2017.

Recently, cell therapies have gained attention as fundamental treatments for epidermolysis bullosa, but their mechanism of action is not fully understood. In this study, we focused on the chemokines that were suggested to related in the migration of bone marrow-derived cells. With the support of other facilities in Japan, which provided sera, the results from the study of sera, skin and epidermal keratinocytes revealed that the serum levels of CCL21, HMGB1 and CXCL12 for the patient group were significantly differ from those for the ontrol group. In addition, the serum levels of CXCL12 and CCL27 tended to differ according to the largeness of the affected area. No previous reports had investigated the chemokines in 45 patients with epidermolysis bullosa, which is a rare disease. These results promise to contribute to efficient cell therapies and to the elucidation of the wound-healing mechanism. This research gave me a different perspective on the Department of Dermatology and reaffirmed the profoundness of our field. I’d like to express my deep appreciation to Professor Shimizu, Dr. Fujita, the other doctors and laboratory technicians who have been instructing me.

Download 'My dissertation' in the annual report 2018, (, 964KB)

Yuka Ohguchi

Gentamicin-induced readthrough and nonsense-mediated mRNA decay of SERPINB7 nonsense mutant transcripts.
Ohguchi Y et al., J Invest Dermatol 138: 836-843, 2018.

In the read-through phenomenon, a nonsense mutation is read through during translation by the ribosome. However, not all nonsense mutations are always read through, and the most important part of clinically applying read-through treatments is to determine whether the nonsense mutation and disorder can be easily read through. In this paper, we hypothesized that Nagashima-type palmoplantar keratosis is an ideal target for read-through treatments, and we proved this to be true. I owe it to Dr. Nomura, Professor Shimizu and all the other members in the laboratory and the department that I was able to research such a clear story and sum it up in the paper. I have great appreciation for them. I sincerely hope our paper will contribute to the treatment of hereditary skin disorders.

Download 'My dissertation' in the annual report 2018, (, 882KB)

Ellen Toyonaga

C-Terminal Processing of Collagen XVII Induces Neoepitopes for Linear IgA Dermatosis Autoantibodies.
Toyonaga E et al, J Invest Dermatol 137: 2552-2559, 2017.

Linear IgA dermatosis (LAD) has been found to be induced by autoimmune antibodies to neoepitopes created by the cleavage of type XVII collagen (COL17). However, the details of this mechanism have not been elucidated. In this study, we produced antibodies similar to autoantibodies of LAD patients and used various methods to confirm that the cleavage changes the structure of COL17 and develops neoepitopes. Most of the experiments we performed showed results that support this theory. We also found that LAD autoantibodies react with COL17 whose C-terminus has been deleted and that neoepitopes produced by the cleavage may be involved in the occurrence of LAD. We expect that an ELISA which uses COL17 with a shortened C-terminus can be used in clinical practice as a system for easy and rapid detection of LAD antibodies. I truly appreciate my mentor Dr. Nishie, who gave me fully support and instructed me throughout the whole project. I hope these research findings will help to elucidate the pathomechanism of LAD.

Download 'My dissertation' in the annual report 2018, (, 1.6MB)

Mika Watanabe

Type XVII collagen coordinates proliferation in the interfollicular epidermis.
Watanabe M et al., eLife 6: e26635, 2017.

My theme in graduate school was the analysis of epidermal phenotypes in type XVII collagen (COL17) knockout mouse. The roles of COL17 in hair follicle stem cells have been elucidated, but those in the interfollicular epidermis have yet to be found. At first, I predicted that the epidermis would be thinner after the loss of COL17 expression than before such loss. However, the result was the opposite: The loss of COL17 expression led to interfollicular epidermal hypertrophy in neonatal mice owing to aberrant Wnt signaling. In addition, I focused on how COL17 works in aging, because COL17 knockout mice express the phenotype of premature aging. COL17 residing in the apico-lateral portion of basal cells was found to decrease, which induced epidermal proliferation. I haven’t always been able to get results in my research, but I feel a precious joy whenever I discover something new, however modest it might be. I’d like to express my deep appreciation to Dr. Ken Natsuga, who has guided me, and to the other doctors in the lab on the 3rd floor, the coauthors of my study, the lab techs and Professor Hiroshi Shimizu.

Download 'My dissertation' in the annual report 2018, (, 1.2MB)

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Hiroshi Shimizu
(Professor & Chairman)
Wataru Nishie
(Senior associate professor)
Yasuyuki Fujita
(Associate professor)
Hideyuki Ujiie
(Associate professor)
Toshifumi Nomura
(Associate professor)
Ken Natsuga
(Associate professor)
Hiroo Hata
(Associate professor)
Hiroaki Iwata
(Associate professor)
Teruki Yanagi
(Assistant professor)
Publications of Faculty Staff
Hiroshi Shimizu
(Professor & Chairman)
Wataru Nishie
(Senior associate professor)
Yasuyuki Fujita
(Associate professor)
Hideyuki Ujiie
(Associate professor)
Toshifumi Nomura
(Associate professor)
Ken Natsuga
(Associate professor)
Hiroo Hata
(Associate professor)
Hiroaki Iwata
(Associate professor)
Teruki Yanagi
(Assistant professor)

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