Molecular and cellular regulation of pancreatic acinar cell function

Abstract

This review focuses on studies from the past year that have greatly advanced our understanding of molecular and cellular regulation of pancreatic acinar cell function. Recent advances focus on signals dictating pancreatic development, acinar cell fate, pancreatic growth, and secretion. Regeneration of acinar cells after pancreatitis depends on expression of embryonic signals in mature acinar cells. In this setting, acinar cells can also transdifferentiate into adipose cells. With the forced induction of certain early and endocrine-driving transcription factors, acinar cells can also transdifferentiate into beta-cells. There has also been an increased understanding of acinar-to-ductal metaplasia and the subsequent formation of pancreatic intraepithelial neoplasia lesions. Multiple proteins involved in secretion have been characterized, including small guanosine triphosphate-binding proteins, soluble N-ethylmaleimide-sensitive factor attachment proteins, and ion channels. These findings demonstrate the regenerative potential of the acinar cell to mitigate injurious states such as pancreatitis. The ability of acinar cells to transdifferentiate into beta-cells could potentially provide a treatment for diabetes. Finally, the results might be helpful in preventing malignant transformation events arising from the acinar cell. Developments in proteomics and computer modeling could expand our view of proteins mediating acinar cell function.