Calcium oscillations induced by ATP in human umbilical cord smooth muscle cells

Research output: Contribution to journalArticle

Standard

Calcium oscillations induced by ATP in human umbilical cord smooth muscle cells. / Meng, Fei; To, Wilson; Kirkman-Brown, Jackson; Kumar, Prem; Gu, Yuchun.

In: Journal of Cellular Physiology, Vol. 213, No. 1, 01.10.2007, p. 79-87.

Research output: Contribution to journalArticle

Harvard

APA

Vancouver

Author

Bibtex

@article{27ce6a65beb642a1983f5d151d624821,
title = "Calcium oscillations induced by ATP in human umbilical cord smooth muscle cells",
abstract = "Arterial smooth muscle cells exhibit vasomotion, related to oscillations in intracellular Ca2+ concentration, but the origin and function of these has not yet been fully determined. We measured intracellular Ca2+ using conventional fluorescent methods in primary cultured, human umbilical cord artery smooth muscle cells (HUCASMC). Spontaneous oscillations in Ca2+ was found in only 1% of all cells but exogenous, micromolar concentrations of ATP could induce Ca2+ oscillations in 70% of cells with the most common pattern being one of regular amplitude and frequency with a return to basal levels between each peak. The P2Y agonist, UTP, but not the P2X agonist alpha beta-methylene ATP, could also induce Ca2+ oscillations. Once induced, these oscillations could not be blocked by G-protein, PLC, VGCC or TRP channel antagonists applied individually, but could be prevented when antagonists were applied together. In the presence of EGTA, micromolar concentrations of ATP induced an elevation in intracellular Ca2+ but did not induce Ca2+ oscillations. The oscillation frequency induced by ATP was affected by bath Ca2+ concentration. Taken together, these data suggest that external Ca2+ entry maintains the Ca2+ oscillation induced by activation of P2Y receptors. Once induced, multiple mechanisms are involved to maintain the oscillation and the oscillation frequency is determined by the speed of Ca2+ refilling. Chronic hypoxia enhanced the Ca2+ response and altered the oscillation frequency. We suggest that these oscillations may play a role in the maintenance of umbilical blood flow during situations in which GPCR are activated.",
author = "Fei Meng and Wilson To and Jackson Kirkman-Brown and Prem Kumar and Yuchun Gu",
year = "2007",
month = oct,
day = "1",
doi = "10.1002/jcp.21092",
language = "English",
volume = "213",
pages = "79--87",
journal = "Journal of Cellular Physiology",
issn = "0021-9541",
publisher = "Wiley",
number = "1",

}

RIS

TY - JOUR

T1 - Calcium oscillations induced by ATP in human umbilical cord smooth muscle cells

AU - Meng, Fei

AU - To, Wilson

AU - Kirkman-Brown, Jackson

AU - Kumar, Prem

AU - Gu, Yuchun

PY - 2007/10/1

Y1 - 2007/10/1

N2 - Arterial smooth muscle cells exhibit vasomotion, related to oscillations in intracellular Ca2+ concentration, but the origin and function of these has not yet been fully determined. We measured intracellular Ca2+ using conventional fluorescent methods in primary cultured, human umbilical cord artery smooth muscle cells (HUCASMC). Spontaneous oscillations in Ca2+ was found in only 1% of all cells but exogenous, micromolar concentrations of ATP could induce Ca2+ oscillations in 70% of cells with the most common pattern being one of regular amplitude and frequency with a return to basal levels between each peak. The P2Y agonist, UTP, but not the P2X agonist alpha beta-methylene ATP, could also induce Ca2+ oscillations. Once induced, these oscillations could not be blocked by G-protein, PLC, VGCC or TRP channel antagonists applied individually, but could be prevented when antagonists were applied together. In the presence of EGTA, micromolar concentrations of ATP induced an elevation in intracellular Ca2+ but did not induce Ca2+ oscillations. The oscillation frequency induced by ATP was affected by bath Ca2+ concentration. Taken together, these data suggest that external Ca2+ entry maintains the Ca2+ oscillation induced by activation of P2Y receptors. Once induced, multiple mechanisms are involved to maintain the oscillation and the oscillation frequency is determined by the speed of Ca2+ refilling. Chronic hypoxia enhanced the Ca2+ response and altered the oscillation frequency. We suggest that these oscillations may play a role in the maintenance of umbilical blood flow during situations in which GPCR are activated.

AB - Arterial smooth muscle cells exhibit vasomotion, related to oscillations in intracellular Ca2+ concentration, but the origin and function of these has not yet been fully determined. We measured intracellular Ca2+ using conventional fluorescent methods in primary cultured, human umbilical cord artery smooth muscle cells (HUCASMC). Spontaneous oscillations in Ca2+ was found in only 1% of all cells but exogenous, micromolar concentrations of ATP could induce Ca2+ oscillations in 70% of cells with the most common pattern being one of regular amplitude and frequency with a return to basal levels between each peak. The P2Y agonist, UTP, but not the P2X agonist alpha beta-methylene ATP, could also induce Ca2+ oscillations. Once induced, these oscillations could not be blocked by G-protein, PLC, VGCC or TRP channel antagonists applied individually, but could be prevented when antagonists were applied together. In the presence of EGTA, micromolar concentrations of ATP induced an elevation in intracellular Ca2+ but did not induce Ca2+ oscillations. The oscillation frequency induced by ATP was affected by bath Ca2+ concentration. Taken together, these data suggest that external Ca2+ entry maintains the Ca2+ oscillation induced by activation of P2Y receptors. Once induced, multiple mechanisms are involved to maintain the oscillation and the oscillation frequency is determined by the speed of Ca2+ refilling. Chronic hypoxia enhanced the Ca2+ response and altered the oscillation frequency. We suggest that these oscillations may play a role in the maintenance of umbilical blood flow during situations in which GPCR are activated.

U2 - 10.1002/jcp.21092

DO - 10.1002/jcp.21092

M3 - Article

C2 - 17477379

VL - 213

SP - 79

EP - 87

JO - Journal of Cellular Physiology

JF - Journal of Cellular Physiology

SN - 0021-9541

IS - 1

ER -