Wang Laboratory

Dr. Wang works in her lab with students
Dr. Wang (center) working with students in her lab.

Islet cell transplantation is the most potent therapy for patients with type 1 diabetes. However, there are two major problems besetting this process.  First, there are not enough islets available for transplant. Second, islets after transplantation are often undergoing apoptosis due to the stresses encountered during islet harvest and after transplantation. The ongoing projects in the Islet Cell Transplantation lab led by Dr. Hongjun Wang are focused on solving these problems.

The areas of investigation in the Wang lab include:

  • New clinical trial explores new therapeutic for type 1 diabetes - To learn more about the clinical trial, visit  www.stemcelldiabetes.com

The clinical trial hypothesis is that systemic administration of MSCs freshly expanded ex vivo reduces progression of diabetes and preserves insulin secretion through restoring normal function of the immune system and preservation/improvement of pancreatic cells in patients with T1D.  

  • generation of insulin-secreting cells from adipose stem cells to expand the source of transplanted islets
  • mechanisms that lead to islet death after allogeneic and autologous islet transplantation
  • interventional approaches that can protect islets from apoptosis and immune rejection by induction of protective genes or encapsulating islets with nanoparticles
  • the role of HO-1 in obesity and insulin resistancea translational approach that can prevent the onset of surgical diabetes after total pancreatectomy
  • islet autotransplantation for patients with chronic pancreatitis

Principal Investigator:

Hongjun Wang, PhD

Research Focus:

The Wang lab focuses on pancreatic islet cell biology and transplantation immunology in the treatment of type 1 and type 2 diabetes and chronic pancreatitis.

Type 1 diabetes: Islet cell transplantation is the most potent therapy for patients with type 1 diabetes. However, there are two major problems besetting this process. First, there are not enough islets available for transplant. Second, islets after transplantation are often undergoing apoptosis due to the stresses encountered during islet harvest and after transplantation and the consequent immune rejection response, thus their function are compromised. Ongoing projects in the Wang lab focus on solving these problems. Major areas of investigation include:

(i)   The roles of a protective gene, heme oxygenase-1 (HO-1) and its products, carbon monoxide and bilirubin in islet transplantation;

(ii)  Generation of insulin-secreting cells from adult stem cells (e.g., adipose stem cells, umbilical cord stem cells) to expand source of transplanted islets;

(iii) Developing novel encapsulation methods using FDA approved nanoparticles to protect islets from apoptosis and immune rejection;

(iv) Understanding the role of the Regulator of G Protein Signaling 2 (RGS2) in islet regeneration.

Chronic Pancreatitis (CP):  CP is a long-standing inflammation of the pancreas that alters its normal structure and functions. Current therapies for CP patients focus on pain relief medically, endoscopically and surgically (by resection of diseased parenchyma and drainage of obstructed ducts). In patients with intractable pain and those with diffuse small duct diseases, total pancreatectomy with islet autotransplantation (TP-IAT) can be an ideal treatment option. Compared to other treatment options for CP, TP-IAT has a higher potential to eliminate pancreatic pain without total sacrifice of the endocrine function of the pancreas. Together with Drs. David B Adams and Katherine A Morgan, we are developing interventional procedures including induction of protective genes, nano-encapsulation, and co-transplantation with mesenchymal stem cells to improve islet yield quantity and quality in order to prevent onset of surgical diabetes after TP-IAT in patients with chronic pancreatitis.

Type 2 diabetes:  Prevalence of obesity has become a social and economic burden for health care today. In addition, obesity is a major cause for insulin resistance and type 2 diabetes (T2D). We have found that HO-1 induction or bilirubin administration reduce hyperglycemia, increases insulin sensitivity in both the leptin-receptor deficient (db/db) mice and the diet-induced obese mice. The goal of our study is to further understand the molecular mechanisms of HO-1 and bilirubin, and to develop clinical applicable therapies to improve obesity and insulin resistance.