九州大学 · 医学
本研究室では、歯由来幹細幹細胞(SHEDやDPSC)の機能とその応用を軸に、骨・歯再生医療や自己免疫疾患の治療戦略の確立を目指しています。特に、SHEDが分泌する非コーディングRNAやエクストラセルラーヴェスキュール(EV)を介した細胞間コミュニケーションが、骨髄間質幹細幹細胞のテロメラーゼ活性を調節することで、閉経後骨量減少の治療に寄与することを解明しています。また、自己免疫疾患モデルマウスにおける幹細胞の免疫調節機能や、疾患由来幹細胞(IP-DPSCs)の再生能の特徴についても、臨床応用に向けた基盤を構築しています。
Figures are computed from collected data and may differ slightly.
Collectively, our findings suggest that SHED-secreted RNAs, such as microRNAs, play a crucial role in treating postmenopausal osteoporosis by targeting the telomerase activity of recipient BMMSCs.
Clinically, irreversible pulpitis is treated by the complete removal of pulp tissue followed by replacement with artificial materials. There is considered to be a high potential for autologous transplantation of human dental pulp stem cells (DPSCs) in endodontic treatment. The usefulness of DPSCs isolated from healthy teeth is limited. However, DPSCs isolated from diseased teeth with irreversible pulpitis (IP-DPSCs) are considered to be suitable for dentin/pulp regeneration. In this study, we ex
Nitric oxide (NO) is thought to play a pivotal regulatory role in dental pulp tissues under both physiological and pathological conditions. However, little is known about the NO functions in dental pulp stem cells (DPSCs). We examined the direct actions of a spontaneous NO gas-releasing donor, NOC-18, on the odontogenic capacity of rat DPSCs (rDPSCs). In the presence of NOC-18, rDPSCs were transformed into odontoblast-like cells with long cytoplasmic processes and a polarized nucleus. NOC-18 tre
Systemic transplantation of stem cells from human exfoliated deciduous teeth (SHED) is used to treat systemic lupus erythematosus (SLE)-like disorders in MRL/<i>lpr</i> mice. However, the mechanisms underlying the SHED-based therapy remain unclear. In this study, we hypothesized that trophic factors within SHED-releasing extracellular vesicles (SHED-EVs) ameliorate the SLE-like phenotypes in MRL/<i>lpr</i> mice. SHED-EVs were isolated from the culture supernatant of SHED. SHED-EVs were treated w
Recent advances in mesenchymal stem/stromal cell (MSC) research have led us to consider the feasibility of MSC-based therapy for various diseases. Human dental pulp-derived MSCs (hDPSCs) have been identified in the dental pulp tissue of deciduous and permanent teeth, and they exhibit properties with self-renewal and in vitro multipotency. Interestingly, hDPSCs exhibit superior immunosuppressive functions toward immune cells, especially T lymphocytes, both in vitro and in vivo. Recently, hDPSCs h
These findings indicate that BA-SHED are not feasible source for BA treatment, because BA-SHED may epigenetically modify the underlying prenatal and perinatal BA environments. In conclusion, these findings suggest that BA-SHED-based studies may provide a platform for understanding the underlying molecular mechanisms of BA development and innovative novel modalities in BA research and treatment.
These findings suggest that targeting hepatic ROS provides a novel approach to treat bone loss resulting from chronic liver diseases.
Human dental pulp stem cell (hDPSCs)-based therapy is a feasible option for regenerative medicine, such as dental pulp regeneration. Here, we show the steps needed to colony-forming unit-fibroblasts (CFU-F)-based isolation, expansion, and cryopreservation of hDPSCs for manufacturing clinical-grade products under a xenogeneic-free/serum-free condition. We also demonstrate the characterization of hDPSCs by CFU-F, flow cytometric, and <i>in vitro</i> multipotent assays. For complete details on the
Systemic transplantation of mesenchymal stem cells (MSCs), such as bone marrow MSCs (BMMSCs) and stem cells from human exfoliated deciduous teeth (SHED), is considered a prominent treatment for osteopenia. However, the mechanism of action of the transplanted MSCs has been poorly elucidated. In the recipient target tissue, including bone and bone marrow, only a few donor MSCs can be detected, suggesting that the direct contribution of donor MSCs may not be expected for osteopenia treatment. Meanw
The present epigenetic memory in BA-SHED implies that BA-SHED imprint bile duct deficiency through TGFBR2 dysregulated by the HNF6 promoter activation epigenetically. Thus, BA-SHED are a potential model for expanding our knowledge in BA research.
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