Lab Team

Islet transplantation is an ideal treatment to cure diabetes and total pancreatectomy with auto-islet transplantation patients. Most islet cells die immediately post transplantation due to hypoxia and innate inflammatory responses. By preventing the islet cell death after transplantation, the patient will have more chance to get insulin-free. Even though taking exogenous insulin can help to control the blood glucose level, the metabolic disorder still can’t improve. My current research is studying the mechanism of clinical therapies and islet cell biology.

The generation of insulin-producing pancreatic β-cells and islet organoids from pluripotent stem cells (PSCs) promises to provide cell sources for diabetes cell replacement therapy. Human PSCs can be induced into glucose-responsive insulin-secreting cells in vitro and transplantation of these cells ameliorates hyperglycemia in diabetic mice. However, the glucose-stimulated insulin-secreting capacity of most cells is still low compared with endogenous islets, therefore suggesting the need to improve induction procedures and cell maturation. The investigation of β-cells formation contributes to the improvement of their proper growth and functioning. My projects focus on the molecular basis of β-cell development and maturation by generating fibroblast or peripheral blood mononuclear cell (PBMC)-derived human induced PSCs (hiPSCs) with a reporter protein and differentiation of hiPSCs into pancreatic β-cells. We are currently trying to identify the role of metabolism shift and the relative molecules in the earliest stage of differentiation.

34.2 million people in the United States have diabetes, with 7.3 million people being undiagnosed! It accounts for more that 300 billion dollars of medical cost. It is clear that diabetes has increasingly become a worldwide health problem, causing a huge burden on the healthcare system and economy. The recent progress in regenerative medicine, especially stem cell therapy, has suggested several novel and potential cures for diabetes, such as the use of Induced Pluripotent Stem Cells which have the ability to exhibit the morphology, growth, marker expression, and pluripotency of embryonic cells. For this project we have chosen human Peripheral Blood Mononuclear Cells to reprogram. The goal of this project is for iPSC to differentiate into Pancreatic β-Cells and investigate the potential mechanism of diabetes in cells and our mouse model.

Dr. Judong Kim earned his PhD from Konkuk University in Seoul, Korea, and specializes in immunology, focusing on autoimmune diseases, particularly type 1 diabetes (T1D). His research examines the roles of T cells and B cells in autoimmune responses, as well as the mechanisms by which mesenchymal stem cells (MSCs) suppress immune function. He is particularly interested in how MSC mitochondria contribute to immune modulation in T1D and their potential impact on disease progression. Dr. Kim's work aims to identify novel therapeutic strategies for regulating immune responses in T1D. He joined the Wang Lab in 2023 as a Staff Scientist I.

I graduated from Clemson University in 2020 with a B.S. in Biological Sciences and a Minor in Chemistry. I contribute to our lab's research on therapies for chronic pancreatitis and type 1 diabetes, specializing in mouse handling, immunohistochemistry, cell culture, and sample processing for our clinical trials. Additionally, I oversee the general maintenance of the lab to ensure it is running smoothly. To further my education, I am currently pursuing a Master's in Analytics at Georgia Tech.

I received my bachelor's degree from Clemson University in 2023, majoring in Health Science with a double minor in Biochemistry and Chemistry. I assist with general lab management as well as benchwork related to our clinical trials and research studies. It is a privilege to support the lab in its endeavors in diabetes and chronic pancreatitis research.