Data from: Nitric oxide signals are interlinked with calcium signals in normal pancreatic stellate cells upon oxidative stress and inflammation

The mammalian diffuse stellate cell system comprises retinoid-storing
cells capable of remarkable transformations from a quiescent to an
activated myofibroblast-like phenotype. Activated pancreatic stellate
cells (PSCs) attract attention owing to the pivotal role they play in
development of tissue fibrosis in chronic pancreatitis and pancreatic
cancer. However, little is known about the actual role of PSCs in the
normal pancreas. These enigmatic cells have recently been shown to respond
to physiological stimuli in a manner that is markedly different from their
neighbouring pancreatic acinar cells (PACs). Here, we demonstrate the
capacity of PSCs to generate nitric oxide (NO), a free radical messenger
mediating, for example, inflammation and vasodilatation. We show that
production of cytosolic NO in PSCs is unambiguously related to cytosolic
Ca2+ signals. Only stimuli that evoke Ca2+ signals in the PSCs elicit
consequent NO generation. We provide fresh evidence for the striking
difference between signalling pathways in PSCs and adjacent PACs, because
PSCs, in contrast to PACs, generate substantial Ca2+-mediated and
NOS-dependent NO signals. We also show that inhibition of NO generation
protects both PSCs and PACs from necrosis. Our results highlight the
interplay between Ca2+ and NO signalling pathways in cell–cell
communication, and also identify a potential therapeutic target for
anti-inflammatory therapies.