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Hypoxic regulation of Ca2+ signaling in cultured rat astrocytes.
Glia. 2005 Jan 01; 49(1):153-7.GLIA

Abstract

Acute hypoxia modulates various cell processes, such as cell excitability, through the regulation of ion channel activity. Given the central role of Ca2+ signaling in the physiological functioning of astrocytes, we have investigated how acute hypoxia regulates such signaling, and compared results with those evoked by bradykinin (BK), an agonist whose ability to liberate Ca2+ from intracellular stores is well documented. In Ca2+-free perfusate, BK evoked rises of [Ca2+]i in all cells examined. Hypoxia produced smaller rises of [Ca2+]i in most cells, but always suppressed subsequent rises of [Ca2+]i induced by BK. Thapsigargin pre-treatment of cells prevented any rise of [Ca2+]i evoked by either BK or hypoxia. Restoration of Ca2+ to the perfusate following a period of acute hypoxia always evoked capacitative Ca2+ entry. During mitochondrial inhibition (due to exposure to carbonyl cyanide p-trifluromethoxyphenyl hydrazone (FCCP) and oligomycin), rises in [Ca2+]i (observed in Ca2+-free perfusate) evoked by hypoxia or by BK, were significantly enhanced, and hypoxia always evoked responses. Our data indicate that hypoxia triggers Ca2+ release from endoplasmic reticulum stores, efficiently buffered by mitochondria. Such liberation of Ca2+ is sufficient to trigger capacitative Ca2+ entry. These findings indicate that the local O2 level is a key determinant of astrocyte Ca2+ signaling, likely modulating Ca2+-dependent astrocyte functions in the central nervous system.

Authors+Show Affiliations

Institute for Cardiovascular Research, University of Leeds, Leeds, United Kingdom.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15390111

Citation

Smith, I F., et al. "Hypoxic Regulation of Ca2+ Signaling in Cultured Rat Astrocytes." Glia, vol. 49, no. 1, 2005, pp. 153-7.
Smith IF, Boyle JP, Kang P, et al. Hypoxic regulation of Ca2+ signaling in cultured rat astrocytes. Glia. 2005;49(1):153-7.
Smith, I. F., Boyle, J. P., Kang, P., Rome, S., Pearson, H. A., & Peers, C. (2005). Hypoxic regulation of Ca2+ signaling in cultured rat astrocytes. Glia, 49(1), 153-7.
Smith IF, et al. Hypoxic Regulation of Ca2+ Signaling in Cultured Rat Astrocytes. Glia. 2005 Jan 1;49(1):153-7. PubMed PMID: 15390111.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hypoxic regulation of Ca2+ signaling in cultured rat astrocytes. AU - Smith,I F, AU - Boyle,J P, AU - Kang,P, AU - Rome,S, AU - Pearson,H A, AU - Peers,C, PY - 2004/9/25/pubmed PY - 2005/3/22/medline PY - 2004/9/25/entrez SP - 153 EP - 7 JF - Glia JO - Glia VL - 49 IS - 1 N2 - Acute hypoxia modulates various cell processes, such as cell excitability, through the regulation of ion channel activity. Given the central role of Ca2+ signaling in the physiological functioning of astrocytes, we have investigated how acute hypoxia regulates such signaling, and compared results with those evoked by bradykinin (BK), an agonist whose ability to liberate Ca2+ from intracellular stores is well documented. In Ca2+-free perfusate, BK evoked rises of [Ca2+]i in all cells examined. Hypoxia produced smaller rises of [Ca2+]i in most cells, but always suppressed subsequent rises of [Ca2+]i induced by BK. Thapsigargin pre-treatment of cells prevented any rise of [Ca2+]i evoked by either BK or hypoxia. Restoration of Ca2+ to the perfusate following a period of acute hypoxia always evoked capacitative Ca2+ entry. During mitochondrial inhibition (due to exposure to carbonyl cyanide p-trifluromethoxyphenyl hydrazone (FCCP) and oligomycin), rises in [Ca2+]i (observed in Ca2+-free perfusate) evoked by hypoxia or by BK, were significantly enhanced, and hypoxia always evoked responses. Our data indicate that hypoxia triggers Ca2+ release from endoplasmic reticulum stores, efficiently buffered by mitochondria. Such liberation of Ca2+ is sufficient to trigger capacitative Ca2+ entry. These findings indicate that the local O2 level is a key determinant of astrocyte Ca2+ signaling, likely modulating Ca2+-dependent astrocyte functions in the central nervous system. SN - 0894-1491 UR - https://www.unboundmedicine.com/medline/citation/15390111/Hypoxic_regulation_of_Ca2+_signaling_in_cultured_rat_astrocytes_ L2 - https://doi.org/10.1002/glia.20083 DB - PRIME DP - Unbound Medicine ER -