Tokyo Institute of Technology · Medicine
Professor Shoen Kume's research lab focuses on stem cell biology and developmental mechanisms underlying pancreatic organogenesis and β-cell differentiation. The lab investigates signaling pathways—such as IP3-Ca2+ signaling, NOGGIN-mediated patterning, and dopamine receptor modulation—that regulate cell fate decisions in pancreatic progenitors and insulin-producing β-cells. Using human induced pluripotent stem cells (hiPSCs) and mouse models, the lab develops xeno-free differentiation systems to generate functional β-cells for regenerative therapy of diabetes. The work also explores the roles of novel genes like Epiplakin1 in maintaining progenitor cell integrity during pancreas development.
Figures are computed from collected data and may differ slightly.
The inositol 1,4,5-trisphosphate (IP3) receptor is a calcium ion channel involved in the release of free Ca2+ from intracellular stores. For analysis of the role of IP3-induced Ca2+ release (IICR) on patterning of the embryonic body, monoclonal antibodies that inhibit IICR were produced. Injection of these blocking antibodies into the ventral part of early Xenopus embryos induced modest dorsal differentiation. A close correlation between IICR blocking potencies and ectopic dorsal axis induction
Human induced pluripotent stem (hiPS) cells are considered a potential source for the generation of insulin-producing pancreatic β-cells because of their differentiation capacity. In this study, we have developed a five-step xeno-free culture system to efficiently differentiate hiPS cells into insulin-producing cells in vitro. We found that a high NOGGIN concentration is crucial for specifically inducing the differentiation first into pancreatic and duodenal homeobox-1 (PDX1)-positive pancreatic
Epiplakin1 (Eppk1) is a plakin family gene with its function remains largely unknown, although the plakin genes are known to function in interconnecting cytoskeletal filaments and anchoring them at plasma membrane-associated adhesive junction. Here we analyzed the expression patterns of Eppk1 in the developing and adult pancreas in the mice. In the embryonic pancreas, Eppk1+/Pdx1+ and Eppk1+/Sox9+ pancreatic progenitor cells were observed in early pancreatic epithelium. Since Pdx1 expression ove
Understanding the molecular mechanisms that regulate β cell mass and proliferation is important for the treatment of diabetes. Here, we identified domperidone (DPD), a dopamine D2 receptor (DRD2) antagonist that enhances β cell mass. Over time, islet β cell loss occurs in dissociation cultures, and this was inhibited by DPD. DPD increased proliferation and decreased apoptosis of β cells through increasing intracellular cAMP. DPD prevented β cell dedifferentiation, which together highly contribut
Recent success in transplantation of islets raises the hopes of diabetic patients that replacement therapies may be a feasible treatment of their disease. Although several lines of evidence suggest that stem cells exist in the pancreas, it is still technically hard for us to isolate or maintain the stem cells in vitro. The establishment of human embryonic stem (ES) cells has excited scientists regarding their potential medical use in tissue replacement therapy. When applied with appropriate sign
Stem cells are defined as having the ability to self-renew and to generate differentiated cells. During embryogenesis, cells are initially proliferative and pluripotent and then they gradually become restricted to different cell fates. In the adult, tissue stem cells are normally quiescent, but become proliferative upon injury. Knowledge from developmental biology and insights into the properties of stem cells are keys to further understanding and successful manipulation. Here, we first focus on
Open papers in the app to read, cite, and organize with AI.
