Working with cultured cells and an animal model, investigators at Saint Louis University have been advancing work on a new drug that may have the potential for fighting pancreatic fibrosis.
A protein known as transforming growth factor beta (or TGFB) spurs fibrogenesis--described as a "series of cellular actions that cause overproduction of collagen and its resulting scarring."
Using an integrin inhibitor they blocked a gene necessary for TGFB to occur, preventing fibrosis in their animal models while also showing they could shutter the gene in cultured cells.
Now they plan to go on with more work in the field, studying how their inhibitor may impact other cells in the pancreas while working on an oral version of their therapy.
"Although the understanding of the causes of chronic pancreatitis and pancreatic cancer have advanced in the past decade, neither the incidence nor the outcome from these diseases has changed--indicating that large gaps in knowledge remain that have prevented the development of effective preventive and treatment measures," said David Griggs, senior author and director of biology at Saint Louis University's Center for World Health and Medicine.
"In this paper we identified a group of proteins as new and important players in the mechanism of pancreatic fibrogenesis. Using a mouse model of chronic pancreatitis developed in SLU's laboratory, we demonstrated that small molecular compounds developed by SLU's Center for World Health and Medicine can very rapidly arrest the fibrosis process even after it is well underway in the organ."