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J. Biol. Chem., Vol. 259, Issue 22, 13777-13782, Nov, 1984
M Prentki, CB Wollheim and PD Lew
The regulation of Ca2+ transport by intracellular compartments was studied
in digitonin-permeabilized human neutrophils, using a Ca2+- selective
electrode. When incubated in a medium containing ATP and respiratory
substrates, the cells lowered within 6 min the ambient [Ca2+] to a steady
state of around 0.2 microM. A vesicular ATP- dependent and
vanadate-sensitive non-mitochondrial pool maintained this low [Ca2+] level.
In the absence of ATP, a higher Ca2+ steady state of 0.6 microM was seen,
exhibiting the characteristics of a mitochondrial Ca2+ "set point." Both
pools were shown to act in concert to restore the previous ambient [Ca2+]
following its elevation. Thus, the mitochondria participate with the other
pool(s) in decreasing [Ca2+] to the submicromolar range whereas only the
nonmitochondrial pool(s) lowers [Ca2+] to the basal level. The action of
inositol 1,4,5- triphosphate (IP3) which has been inferred to mediate Ca2+
mobilization in a few cell types was studied. IP3 released (detectable
within 2 s) Ca2+ accumulated in the ATP-dependent pool(s) but had no effect
on the mitochondria. The response was transient and resulted in
desensitization toward subsequent IP3 additions. Under experimental
conditions in which the ATP-dependent Ca2+ influx was blocked, the addition
of IP3 resulted in a very large Ca2+ release from nonmitochondrial pool.
The results strongly suggest that IP3 is a second messenger mediating
intracellular Ca2+ mobilization in human neutrophils. Furthermore, the
nonmitochondrial pool appears to have independent influx and efflux
pathways for Ca2+ transport, a Ca2+ ATPase (the influx component) and an
IP3-sensitive efflux component activated during Ca2+ mobilization.
Ca2+ homeostasis in permeabilized human neutrophils. Characterization of Ca2+-sequestering pools and the action of inositol 1,4,5- triphosphate
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