scholarly journals Corrigendum to “Mechanism of voltage-gated channel formation in lipid membranes” [Biochim. Biophys. Acta 1858 (2016) 748–755]

2016 ◽  
Vol 1858 (11) ◽  
pp. 2957 ◽  
Author(s):  
Rolando Guidelli ◽  
Lucia Becucci
Keyword(s):  
Lipid Membranes ◽  
Channel Formation ◽  
Voltage Gated ◽  
Gated Channel

scholarly journals Non-linear Conductance, Rectification, and Mechanosensitive Channel Formation of Lipid Membranes

2021 ◽  
Vol 8 ◽  
Author(s):  
Karis Amata Zecchi ◽  
Thomas Heimburg
Keyword(s):  
Lipid Bilayers ◽  
Lipid Membranes ◽  
Lipid Membrane ◽  
Electrical Response ◽  
Spontaneous Curvature ◽  
Pressure Gradients ◽  
Channel Formation ◽  
Voltage Gated ◽  
Non Linear ◽  
Different Depths

There is mounting evidence that lipid bilayers display conductive properties. However, when interpreting the electrical response of biological membranes to voltage changes, they are commonly considered as inert insulators. Lipid bilayers under voltage-clamp conditions display current traces with discrete conduction-steps, which are indistinguishable from those attributed to the presence of protein channels. In current-voltage (I-V) plots they may also display outward rectification, i.e., voltage-gating. Surprisingly, this has even been observed in chemically symmetric lipid bilayers. Here, we investigate this phenomenon using a theoretical framework that models the electrostrictive effect of voltage on lipid membranes in the presence of a spontaneous polarization, which can be recognized by a voltage offset in electrical measurements. It can arise from an asymmetry of the membrane, for example from a non-zero spontaneous curvature of the membrane. This curvature can be caused by voltage via the flexoelectric effect, or by hydrostatic pressure differences across the membrane. Here, we describe I-V relations for lipid membranes formed at the tip of patch pipettes situated close to an aqueous surface. We measured at different depths relative to air/water surface, resulting in different pressure gradients across the membrane. Both linear and non-linear I-V profiles were observed. Non-linear conduction consistently takes the form of outward rectified currents. We explain the conductance properties by two mechanisms: One leak current with constant conductance without pores, and a second process that is due to voltage-gated pore opening correlating with the appearance of channel-like conduction steps. In some instances, these non-linear I-V relations display a voltage regime in which dI/dV is negative. This has also been previously observed in the presence of sodium channels. Experiments at different depths reveal channel formation that depends on pressure gradients. Therefore, we find that the channels in the lipid membrane are both voltage-gated and mechanosensitive. We also report measurements on black lipid membranes that also display rectification. In contrast to the patch experiments they are always symmetric and do not display a voltage offset.

Inhibiting MicroRNA-497 Improves the Effects of Exercise Training on Myocardial Infarction

2020 ◽  
Vol 41 (07) ◽  
pp. 475-483
Author(s):  
Zhenci Li ◽  
Jing Lv ◽  
Yizhi Pan ◽  
Yi Luo ◽  
Zhen Liu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Exercise Training ◽  
Infarct Size ◽  
Interval Training ◽  
Inflammatory Factors ◽  
Rat Models ◽  
Voltage Gated ◽  
Positive Effects ◽  
Gated Channel ◽  
Positive Effect

AbstractExercise training (ET) could improve myocardial infarction (MI), and microRNA-497 is highly associated with MI. This study aimed to investigate whether the regulation of miR-497 is involved in the positive effects of ET on MI. MI rat models induced by left anterior descending (LAD) were subjected to interval training and infarct size was observed. Blood and myocardial samples were collected from the rats for determining the expressions of miR-497. To evaluate the functions of miR-497, miR-497 agomir and antagomir were injected accordingly into grouped rats during ET, and subsequently, the expressions of apoptotic and inflammatory factors were determined. ET reduced the infarct size in MI rats and inhibited the levels of miR-497. MiR-497 agomir injection enlarged the infarct size, and reversed the shrunk infarct size induced by ET. However, miR-497 antagomir further promoted the positive effect on MI improved by ET. Chloride voltage-gated channel 3 (CLCN3) was identified as the most possible target for miR-497. Moreover, ET improving MI also involved the regulation of apoptotic and inflammatory factors. The mechanisms underlying the positive effects of ET on MI were highly associated with the regulation of miR-497.

Sign in / Sign up

Export Citation Format

Share Document