Effects of cGMP-dependent protein kinase signaling in Drosophila S2 cells subjected to anoxia and oxidative stress

Ischemic stroke is one of the leading causes of human death worldwide. It occurs due to
high susceptibility of neurons to anoxia and reoxygenation. Unlike mammals, invertebrate
Drosophila melanogaster withstands low oxygen levels without showing pathology. In the
present study, Drosophila Schneider (S2) cells were employed to investigate the role of the
cGMP-dependent Protein Kinase (PKG) signaling pathway in Drosophila anoxia-tolerance in
vitro. This was accomplished by subjecting cells to chemical anoxia and oxidative stress
concurrently with treatments by pharmacological agents affecting specific targets of the PKG
pathway and assessing cytotoxicity. In this study, activation of the PKG pathway protected S2
cells from the aforementioned stresses. The results of this study may lead to a better
understanding of fruit fly’s innate anoxia-tolerance strategies. Consequently, this knowledge may
be used to identify potential therapeutic targets to prevent detrimental neurological effects of an
ischemic stroke in humans.