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Abdalah R, Wei L, Francis K, Yu SP.
Valinomycin - induced apoptosis in Chinese hamster ovary
cells.
Neurosci Lett. 2006 Jul 18
Department of Pathology and Laboratory Medicine, Medical
University of South Carolina, Charleston, SC 29425, United
States.
Accumulating evidence endorses that excessive K(+) efflux is an
ionic mechanism underlying apoptosis both in neuronal and
non-neuronal cells. K(+) channels play important roles in
mediating the pro-apoptotic K(+) efflux. Chinese hamster ovary
(CHO) cells have been widely used for gene transfection
experiments. These cells lack detectable endogenous
voltage-gated K(+) channels. We were interested in knowing
whether the absence of endogenous K(+) channels would render
wild-type CHO cells more resistant to apoptotic death. We also
wished to determine if direct stimulation of K(+) efflux would
trigger apoptosis in these cells. Exposing CHO cells to hypoxia
(1% O(2)) or to a typical apoptotic insult of serum deprivation
for up to 24h did not affect cell survival. On the other hand,
the K(+) ionophore valinomycin caused substantial cell death
within 12h of its application. Valinomycin-treated CHO cells
underwent several apoptotic events, including phosphatidylserine
(PS) membrane translocation, caspase-3 activation, and
mitochondrial membrane depolarization during the first few hours
of exposure. Reducing K(+) efflux by elevating extracellular
K(+) concentrations noticeably attenuated valinomycin-induced
cell death. This study reinforces a K(+) efflux-mediated
apoptotic mechanism in CHO cells and may help to explain the
unique feature of their higher tolerance to apoptosis.
PMID: 16857314
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