Premium
Effects of chronic hypoxia on Ca 2+ stores and capacitative Ca 2+ entry in human neuroblastoma (SH‐SY5Y) cells
Author(s) -
Smith I. F.,
Boyle J. P.,
Vaughan P. F. T.,
Pearson H. A.,
Peers C.
Publication year - 2001
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2001.00620.x
Subject(s) - hypoxia (environmental) , intracellular , endocrinology , medicine , sh sy5y , fura 2 , calcium , neuroblastoma , calcium in biology , chemistry , biology , cell culture , biochemistry , genetics , organic chemistry , cytosol , oxygen , enzyme
Microfluorimetric measurements of intracellular calcium ion concentration [Ca 2+ ] i were employed to examine the effects of chronic hypoxia (2.5% O 2 , 24 h) on Ca 2+ stores and capacitative Ca 2+ entry in human neuroblastoma (SH‐SY5Y) cells. Activation of muscarinic receptors evoked rises in [Ca 2+ ] i which were enhanced in chronically hypoxic cells. Transient rises of [Ca 2+ ] i evoked in Ca 2+ ‐free solutions were greater and decayed more slowly following exposure to chronic hypoxia. In control cells, these transient rises of [Ca 2+ ] i were also enhanced and slowed by removal of external Na + , whereas the same manoeuvre did not affect responses in chronically hypoxic cells. Capacitative Ca 2+ entry, observed when re‐applying Ca 2+ following depletion of intracellular stores, was suppressed in chronically hypoxic cells. Western blots revealed that presenilin‐1 levels were unaffected by chronic hypoxia. Exposure of cells to amyloid β peptide (1–40) also increased transient [Ca 2+ ] i rises, but did not mimic any other effects of chronic hypoxia. Our results indicate that chronic hypoxia causes increased filling of intracellular Ca 2+ stores, suppressed expression or activity of Na + /Ca 2+ exchange and reduced capacitative Ca 2+ entry. These effects are not attributable to increased amyloid β peptide or presenilin‐1 levels, but are likely to be important in adaptive cellular remodelling in response to prolonged hypoxic or ischemic episodes.