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A mechanosensitive cation channel in endothelial cells.
Xiaoqiang Yao1, H Y Kwan, Yu Huang
1Department of Physiology, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong, China. yao2068@cuhk.edu.hk
Journal of Cardiac Surgery
|January 28, 2003
Summary
Vascular endothelial cells possess a mechanosensitive channel activated by blood flow. This channel
Area of Science:
- Physiology
- Cell Biology
- Cardiovascular Research
Background:
- Vascular endothelial cells experience mechanical forces from hemodynamic blood flow.
- Calcium (Ca2+) signaling is crucial for endothelial cell function.
- Mechanosensitive ion channels play a role in cellular responses to physical stimuli.
Purpose of the Study:
- To investigate the role of a mechanosensitive cation channel in mediating flow-induced Ca2+ influx in vascular endothelial cells.
- To explore the potential regulation of this channel by cyclic guanosine monophosphate (cGMP) and protein kinase G (PKG).
Main Methods:
- Utilized patch-clamp electrophysiology to study ion channel activity.
- Measured Ca2+ influx in response to controlled fluid shear stress.
- Applied pharmacological inhibitors (Gd3+, Ni2+, SK&F-96365) and cGMP to modulate channel activity.
Main Results:
- Hemodynamic blood flow significantly increased the activity of a mechanosensitive Ca2+-permeable channel in endothelial cells.
- cGMP, via a PKG-dependent pathway, inhibited this channel, abolishing flow-induced Ca2+ influx.
- Specific cation channel inhibitors also blocked flow-induced Ca2+ entry.
Conclusions:
- A mechanosensitive cation channel is identified as the primary mediator of flow-induced Ca2+ entry in vascular endothelial cells.
- cGMP-dependent signaling, involving PKG, acts as a negative regulator of this mechanosensitive channel.