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Hypoxia augments the calcium-activated chloride current carried by anoctamin-1 in cardiac vascular endothelial cells of neonatal mice.

Wu MM, Lou J, Song BL, Gong YF, Li YC, Yu CJ, Wang QS, Ma TX, Ma K, Hartzell HC, Duan DD, Zhao D, Zhang ZR - Br. J. Pharmacol. (2014)

Bottom Line: The density of ICl ( C a) detected in CVECs was significantly inhibited by T16Ainh -A01, an Ano1 inhibitor, and a pore-targeting, specific anti-Ano1 antibody, and was markedly decreased in Ano1 gene knockdown CVECs.Ano1 formed CaCC in CVECs of neonatal mice.Ano1 may play a role in the pathophysiological processes during ischaemia in heart, and therefore, Ano1 might be a potential therapeutic target to prevent ischaemic damage.

View Article: PubMed Central - PubMed

Affiliation: Departments of Clinical Pharmacy and Cardiology, Institute of Clinical Pharmacy, The 2nd Affiliated Hospital, Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, Harbin Medical University, Harbin, China.

No MeSH data available.


Related in: MedlinePlus

(A–F) Representative macroscopic currents were recorded in CVECs, in the presence of desired free [Ca2+]i, with the voltage protocol shown in the inset. (G) Calculated steady-state current densities, in the presence of a variety of free [Ca2+]i, were plotted as a function of membrane potentials (n = 5–11 for different data points). (H) Current densities calculated from tail currents measured at −100 mV after pre-pulses between +100 and −100 mV were plotted against [Ca2+]i and were fitted with the Hill equation (n = 7–11 for different data points).
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fig01: (A–F) Representative macroscopic currents were recorded in CVECs, in the presence of desired free [Ca2+]i, with the voltage protocol shown in the inset. (G) Calculated steady-state current densities, in the presence of a variety of free [Ca2+]i, were plotted as a function of membrane potentials (n = 5–11 for different data points). (H) Current densities calculated from tail currents measured at −100 mV after pre-pulses between +100 and −100 mV were plotted against [Ca2+]i and were fitted with the Hill equation (n = 7–11 for different data points).

Mentions: A group of macroscopic currents was recorded from mouse CVECs in the presence of a variety concentrations of free [Ca2+]i (Fig. 1A–F). The current recorded, in the presence of 18 nM free [Ca2+]i, exhibited no outward rectification and time-dependent relaxation (Fig. 1A and G). The amplitude of the outward currents was amplified gradually and the outward rectification and time-dependent relaxation became more profound, as free [Ca2+]i was increased from 290 nM to 1.1 μM (Fig. 1B–E and G). However, when free [Ca2+]i reached 36.5 μM, the inward and outward currents were nearly equal in amplitude, and time-dependent relaxation was almost lost (Fig. 1F and G). The macroscopic currents were deactivated by switching membrane potential to −100 mV. The average instantaneous tail current density measured at −100 mV after pre-pulses to different membrane voltage was plotted as a function of free [Ca2+]i and the data points were fitted to the Hill equation (Fig. 1H). The data show that EC50 of free [Ca2+]i decreased by about fourfold [2.08 ± 1.04 μM at 0 mV (n = 7–11) vs. 0.53 ± 0.06 μM at +100 mV (n = 7–11)]. These results suggest that the gating of the macroscopic currents recorded from CVECs is Ca2+- and voltage-dependent.


Hypoxia augments the calcium-activated chloride current carried by anoctamin-1 in cardiac vascular endothelial cells of neonatal mice.

Wu MM, Lou J, Song BL, Gong YF, Li YC, Yu CJ, Wang QS, Ma TX, Ma K, Hartzell HC, Duan DD, Zhao D, Zhang ZR - Br. J. Pharmacol. (2014)

(A–F) Representative macroscopic currents were recorded in CVECs, in the presence of desired free [Ca2+]i, with the voltage protocol shown in the inset. (G) Calculated steady-state current densities, in the presence of a variety of free [Ca2+]i, were plotted as a function of membrane potentials (n = 5–11 for different data points). (H) Current densities calculated from tail currents measured at −100 mV after pre-pulses between +100 and −100 mV were plotted against [Ca2+]i and were fitted with the Hill equation (n = 7–11 for different data points).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4128065&req=5

fig01: (A–F) Representative macroscopic currents were recorded in CVECs, in the presence of desired free [Ca2+]i, with the voltage protocol shown in the inset. (G) Calculated steady-state current densities, in the presence of a variety of free [Ca2+]i, were plotted as a function of membrane potentials (n = 5–11 for different data points). (H) Current densities calculated from tail currents measured at −100 mV after pre-pulses between +100 and −100 mV were plotted against [Ca2+]i and were fitted with the Hill equation (n = 7–11 for different data points).
Mentions: A group of macroscopic currents was recorded from mouse CVECs in the presence of a variety concentrations of free [Ca2+]i (Fig. 1A–F). The current recorded, in the presence of 18 nM free [Ca2+]i, exhibited no outward rectification and time-dependent relaxation (Fig. 1A and G). The amplitude of the outward currents was amplified gradually and the outward rectification and time-dependent relaxation became more profound, as free [Ca2+]i was increased from 290 nM to 1.1 μM (Fig. 1B–E and G). However, when free [Ca2+]i reached 36.5 μM, the inward and outward currents were nearly equal in amplitude, and time-dependent relaxation was almost lost (Fig. 1F and G). The macroscopic currents were deactivated by switching membrane potential to −100 mV. The average instantaneous tail current density measured at −100 mV after pre-pulses to different membrane voltage was plotted as a function of free [Ca2+]i and the data points were fitted to the Hill equation (Fig. 1H). The data show that EC50 of free [Ca2+]i decreased by about fourfold [2.08 ± 1.04 μM at 0 mV (n = 7–11) vs. 0.53 ± 0.06 μM at +100 mV (n = 7–11)]. These results suggest that the gating of the macroscopic currents recorded from CVECs is Ca2+- and voltage-dependent.

Bottom Line: The density of ICl ( C a) detected in CVECs was significantly inhibited by T16Ainh -A01, an Ano1 inhibitor, and a pore-targeting, specific anti-Ano1 antibody, and was markedly decreased in Ano1 gene knockdown CVECs.Ano1 formed CaCC in CVECs of neonatal mice.Ano1 may play a role in the pathophysiological processes during ischaemia in heart, and therefore, Ano1 might be a potential therapeutic target to prevent ischaemic damage.

View Article: PubMed Central - PubMed

Affiliation: Departments of Clinical Pharmacy and Cardiology, Institute of Clinical Pharmacy, The 2nd Affiliated Hospital, Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, Harbin Medical University, Harbin, China.

No MeSH data available.


Related in: MedlinePlus