Hokkaido University · Medicine
Professor Yasuyuki Fujita's research lab specializes in regenerative medicine and genetic skin disorders, with a primary focus on epidermolysis bullosa (EB) and other genodermatoses. The lab investigates the therapeutic potential of bone marrow-derived stem cells, particularly Muse cells and hematopoietic stem cell transplantation, to restore structural proteins in EB caused by defects in keratinocyte adhesion molecules such as collagen XVII. Their work also explores immune cell trafficking in skin diseases, including the role of chemokine receptors like CCR10 in mycosis fungoides, and emphasizes translational approaches such as allogeneic cell infusion and gene-corrected stem cell therapy. The lab integrates molecular biology, stem cell biology, and clinical dermatology to develop novel regenerative strategies for severe inherited skin diseases.
Figures are computed from collected data and may differ slightly.
The rate of second-case Kawasaki disease occurring among 1788 siblings of children with the disease was derived from data obtained from questionnaires mailed to the members of the Japanese Association of Parents of Children With Kawasaki Disease. Within 1 year after the onset of the first case in a family, the overall second-case rate was 2.1% for siblings, as compared to an overall incidence of approximately 0.19% in the general population of children 0 to 4 years of age in Japan in the epidemi
URL: https://dbcentre3.jmacct.med.or.jp/jmactr/Default.aspx. Unique identifier: JMA-IIA00022)
Attempts to treat congenital protein deficiencies using bone marrow-derived cells have been reported. These efforts have been based on the concepts of stem cell plasticity. However, it is considered more difficult to restore structural proteins than to restore secretory enzymes. This study aims to clarify whether bone marrow transplantation (BMT) treatment can rescue epidermolysis bullosa (EB) caused by defects in keratinocyte structural proteins. BMT treatment of adult collagen XVII (Col17) kno
Epidermolysis bullosa (EB) is a group of genodermatoses characterized by generalized blisters from mutations in the genes encoding the basement membrane zone (BMZ) proteins.1 The infusion of allogeneic cells such as mesenchymal stem/stromal cells (MSCs), which have intact BMZ genes, is a promising treatment.2-6 We here focus on multilineage-differentiating stress-enduring (Muse) cells, which were initially found as a stem cell marker stage-specific embryonic antigen (SSEA)-3-positive subpopulati
CCR10-CTACK/CCL27 interactions between circulating T cells and keratinocytes would seem to play an important role in the pathophysiology of MF from the early disease stages.
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