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Cholesterol depletion alters coronary artery myocyte Ca(2+) signalling in a stimulus-specific manner.

Prendergast C, Quayle J, Burdyga T, Wray S - Cell Calcium (2010)

Bottom Line: We have examined the effect of the cholesterol-depleting agents, methyl-cyclodextrin (MCD) and cholesterol oxidase, on high K(+), caffeine and agonist-induced Ca(2+) signals.There was also a significant decrease in cell capacitance.These data are discussed in terms of the involvement of caveolae in receptor localisation, Ca(2+) entry pathways and SR Ca(2+) release, and the role of these in agonist signalling.

View Article: PubMed Central - PubMed

Affiliation: University of Liverpool, Merseyside, UK. c.prendergast@liv.ac.uk

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(A) Mean inward current–voltage relationship in the absence and presence of MCD. (B) Representative traces, recorded from the same cell, showing the outward current generated by a +50 mV depolarisation in the absence and presence of MCD. (C) Effect of MCD on outward K+ current and (D) Effect of MCD on cell capacitance.
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fig6: (A) Mean inward current–voltage relationship in the absence and presence of MCD. (B) Representative traces, recorded from the same cell, showing the outward current generated by a +50 mV depolarisation in the absence and presence of MCD. (C) Effect of MCD on outward K+ current and (D) Effect of MCD on cell capacitance.

Mentions: The effect of MCD was also evaluated in electrophysiological studies on freshly isolated coronary artery myocytes. When Cs+ was used in the pipette solution (instead of K+), no outward current was apparent. A small inward current (2.1 ± 0.1 pA/pF) was observed, peaking at 0 mV and sensitive to inhibition with nifedipine and potentiation with Bay K8644 (n = 4, data not shown). Experiments evaluating the effect of cholesterol extraction were carried out in the presence of 1 μM Bay K8644. Treatment with MCD for 10 min did not significantly alter the inward current over the entire voltage range tested, as shown in Fig. 6A (peak current at 0 mV: control 2.66 ± 0.8 pA/pF versus 2.65 ± 0.4 pA/pF, n = 3).


Cholesterol depletion alters coronary artery myocyte Ca(2+) signalling in a stimulus-specific manner.

Prendergast C, Quayle J, Burdyga T, Wray S - Cell Calcium (2010)

(A) Mean inward current–voltage relationship in the absence and presence of MCD. (B) Representative traces, recorded from the same cell, showing the outward current generated by a +50 mV depolarisation in the absence and presence of MCD. (C) Effect of MCD on outward K+ current and (D) Effect of MCD on cell capacitance.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2824115&req=5

fig6: (A) Mean inward current–voltage relationship in the absence and presence of MCD. (B) Representative traces, recorded from the same cell, showing the outward current generated by a +50 mV depolarisation in the absence and presence of MCD. (C) Effect of MCD on outward K+ current and (D) Effect of MCD on cell capacitance.
Mentions: The effect of MCD was also evaluated in electrophysiological studies on freshly isolated coronary artery myocytes. When Cs+ was used in the pipette solution (instead of K+), no outward current was apparent. A small inward current (2.1 ± 0.1 pA/pF) was observed, peaking at 0 mV and sensitive to inhibition with nifedipine and potentiation with Bay K8644 (n = 4, data not shown). Experiments evaluating the effect of cholesterol extraction were carried out in the presence of 1 μM Bay K8644. Treatment with MCD for 10 min did not significantly alter the inward current over the entire voltage range tested, as shown in Fig. 6A (peak current at 0 mV: control 2.66 ± 0.8 pA/pF versus 2.65 ± 0.4 pA/pF, n = 3).

Bottom Line: We have examined the effect of the cholesterol-depleting agents, methyl-cyclodextrin (MCD) and cholesterol oxidase, on high K(+), caffeine and agonist-induced Ca(2+) signals.There was also a significant decrease in cell capacitance.These data are discussed in terms of the involvement of caveolae in receptor localisation, Ca(2+) entry pathways and SR Ca(2+) release, and the role of these in agonist signalling.

View Article: PubMed Central - PubMed

Affiliation: University of Liverpool, Merseyside, UK. c.prendergast@liv.ac.uk

Show MeSH
Related in: MedlinePlus