The Effects of Transforming Growth Factor Beta in Neuronal Innervation in Pancreatitis

Overview

Chronic pancreatitis is characterized by the destruction of the exocrine parenchyma and progressive fibrosis. TGF-beta is a cytokine that has many important functions within the pancreas, including fibrosis and acinar to ductal metaplasia which plays a large role in the development of fibrotic tissue. Not only does TGF-beta af fect the accumulation of fibroblasts and pancreatic stellate cells, but it also upregulates pancreatic sensory neurons in chronic pancreatitis–leading to increased pain. Increased sensory neuronal innervation can also contribute to PDAC tumorigenesis and p erineural invasion, as bi -directional communication between sensory neurons has been shown to promote tumor formation and metastasis. This leads to the following questions: what is the role of TGF -beta in neurotrophic growth in chronic pancreatitis, and how can it affect the formation and growth of pancreatic ductal adenocarcinoma (PDAC).? By disrupting TGF -beta signaling in acinar cells, we can observe how the pancreatic micro -environment changes using immunofluorescence to visualize and quantify the amount of neuronal innervation. I hypothesized that by knocking out the TGF -beta signaling pathway, the level of nerve innervation will decrease. Preliminary results demonstrate that while there is a difference between the control and TGF - beta knockout mice, due to the heterogeneous nature of the i nflammation in the pancreas it is difficult to quantify the changes in the nerve morphology without bias. With the knowledge of how exocrine -derived TGF-beta signaling affects neuronal innervation and inflammation, we can better understand neuropathy in pancreatitis and how it can lead to pancreatic cancer. Greater Washington, D.C.

Competition history

• JSHS 2024 Category not listed

Resources

• National JSHS abstract book ↗

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