Effects of chronic hypoxia on Ca[sup 2+] stores and capacitative Ca[sup 2+] entry in human neuroblastoma (SH-SY5Y) cells.

Autor: Smith, I.F., Boyle, J.P., Vaughan, P.F.T., Pearson, H.A., Peers, C.
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Zdroj: Journal of Neurochemistry; 11/15/2001, Vol. 79 Issue 4, p877-884, 8p, 23 Graphs
Abstrakt: Microfluorimetric measurements of intracellular calcium ion concentration [Ca[sup 2+]][sub i] were employed to examine the effects of chronic hypoxia (2.5% O[sub 2], 24 h) on Ca[sup 2+] stores and capacitative Ca[sup 2+] entry in human neuroblastoma (SH-SY5Y) cells. Activation of muscarinic receptors evoked rises in [Ca[sup 2+]][sub i] which were enhanced in chronically hypoxic cells. Transient rises of [Ca[sup 2+]][sub i] evoked in Ca[sup 2+]-free solutions were greater and decayed more slowly following exposure to chronic hypoxia. In control cells, these transient rises of [Ca[sup 2+]][sub i] were also enhanced and slowed by removal of external Na[sup +], whereas the same manoeuvre did not affect responses in chronically hypoxic cells. Capacitative Ca[sup 2+] entry, observed when re-applying Ca[sup 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[sup 2+]][sub i] rises, but did not mimic any other effects of chronic hypoxia. Our results indicate that chronic hypoxia causes increased filling of intracellular Ca[sup 2+] stores, suppressed expression or activity of Na[sup +]/Ca[sup 2+] exchange and reduced capacitative Ca[sup 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. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index
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