Yamaza H. . Bilirubin induces discoloration and hypodontia on tooth . Pediatric Dental Journal32 ( 1 ) 1 - 5 2022年4月 詳細を見る 記2022 · 記述言語： 日本語 出版者・発行元： Pediatric Dental Journal Background: Systematic and local factors give various effects to teeth during odontogenesis or after eruption. Discoloration of teeth is also caused by systematic and local factors and sometimes leads to esthetic and biological problems. Bilirubin is the product of heme metabolism and causes greenish discoloration and hypodontia with its high concentration in blood. Objective: This review aimed to indicate effects of bilirubin on odontogenesis with in vitro model established by stem cells of human exfoliated deciduous teeth (SHED). Results: Recent studies showed that bilirubin suppressed cell proliferation and promoted cell death in SHED with alteration of their involved-signaling pathways. In addition, it was indicated that pamidronate recovered bilirubin-altered signaling pathways and bilirubin-impaired dentinogenic function of SHED. Conclusion: SHED could be tool to established human in vitro model to elucidate human pathogenesis and for screening to pick up the candidates of medicines. DOI： 10.1016/j.pdj.2021.11.002 Scopus
Yamada A., Yoshizaki K., Saito K., Ishikawa M., Chiba Y., Hoshikawa S., Chiba M., Hino R., Maruya Y., Sato H., Masuda K., Yamaza H., Nakamura T., Iwamoto T., Fukumoto S. . GSK3beta inhibitor-i2022 · 記述言語： 日本語 出版者・発行元： Journal of Oral Biosciences Objectives: Epithelial-mesenchymal interactions are extremely important in tooth development and essential for ameloblast differentiation, especially during tooth formation. We aimed to identify the type of mesenchymal cells important in ameloblast differentiation. Methods: We used two types of cell culture systems with chambers and found that a subset of debtal mesenchimal cells is important for the differentiatiuon of dental spithelial cells into ameloblasts. Further, we induced dental pulp stem cell-like cells from dental pulp stem cells using the small molecule compound BIO ( a GSK-3 inhibitor IX) to clarify the mechanism involved in ameloblast differentiation induced by dental pulp stem cells. Results: The BIO-induced dental pulp cells promoted the expression of mesenchymal stem cell markers Oct3/4 and Bcrp1. Furthermore, we used artificial dental pulp stem cells induced by BIO to identify the molecules expressed in dental pulp stem cells required for ameloblast differentiation. Panx3 expression was induced in the dental pulp stem cell through interaction with the dental epithelial cells. In addition, ATP release from cells increased in Panx3-expressing cells. We also confirmed that ATP stimulation is accepted in dental epithelial cells. Conclusions: These results showed that the Panx3 expressed in dental pulp stem cells is important for ameloblast differentiation and that ATP release by Panx3 may play a role in epithelial–mesenchymal interaction. DOI： 10.1016/j.job.2022.10.002 Scopus PubMed
Sonoda S., Murata S., Yamaza H., Yuniartha R., Fujiyoshi J., Yoshimaru K., Matsuura T., Oda Y., Ohga S., Tajiri T., Taguchi T., Yamaza T. . Targeting hepatic oxidative stress rescues bone loss2022 · 記述言語： 日本語 出版者・発行元： Molecular Metabolism Objective: Chronic liver diseases often involve metabolic damage to the skeletal system. The underlying mechanism of bone loss in chronic liver diseases remains unclear, and appropriate therapeutic options, except for orthotopic liver transplantation, have proved insufficient for these patients. This study aimed to investigate the efficacy and mechanism of transplantation of immature hepatocyte-like cells converted from stem cells from human exfoliated deciduous teeth (SHED-Heps) in bone loss of chronic liver fibrosis. Methods: Mice that were chronically treated with CCl4 received SHED-Heps, and trabecular bone density, reactive oxygen species (ROS), and osteoclast activity were subsequently analyzed in vivo and in vitro. The effects of stanniocalcin 1 (STC1) knockdown in SHED-Heps were also evaluated in chronically CCl4 treated mice. Results: SHED-Hep transplantation (SHED-HepTx) improved trabecular bone loss and liver fibrosis in chronic CCl4-treated mice. SHED-HepTx reduced hepatic ROS production and interleukin 17 (Il-17) expression under chronic CCl4 damage. SHED-HepTx reduced the expression of both Il-17 and tumor necrosis factor receptor superfamily 11A (Tnfrsf11a) and ameliorated the imbalance of osteoclast and osteoblast activities in the bone marrow of CCl4-treated mice. Functional knockdown of STC1 in SHED-Heps attenuated the benefit of SHED-HepTx including anti-bone loss effect by suppressing osteoclast differentiation through TNFSF11–TNFRSF11A signaling and enhancing osteoblast differentiation in the bone marrow, as well as anti-fibrotic and anti-ROS effects in the CCl4-injured livers. Conclusions: These findings suggest that targeting hepatic ROS provides a novel approach to treat bone loss resulting from chronic liver diseases. DOI： 10.1016/j.molmet.2022.101599 Scopus PubMed
