TRPV2 modulates mechanically Induced ATP Release from Human bronchial epithelial cells

Area of Science:

• Cell Biology
• Physiology
• Ion Channel Research

Background:

• Coughing generates significant shear stress in the airways.
• This mechanical stress can lead to the release of alarmins and adenosine triphosphate (ATP).
• Ion channels are potential modulators of this ATP release mechanism.

Purpose of the Study:

• To investigate the role of the transient receptor potential vanilloid member 2 (TRPV2) channel.
• To determine if TRPV2 influences mechanically induced ATP release from human primary bronchial epithelial cells (PBECs).

Main Methods:

• PBECs were subjected to mechanical stress (compressive and fluid shear stress or fluid shear stress alone).
• ATP release was quantified using a luciferin-luciferase assay.
• TRPV2 function was assessed using calcium imaging, and its inhibition was studied with tranilast or siRNA knockdown.

Main Results:

• Mechanical stress significantly increased ATP release from PBECs.
• Functional TRPV2 channels were detected in PBECs and TRPV2 protein was present in human lung tissue.
• Inhibition of TRPV2, via tranilast or siRNA, significantly reduced mechanically induced ATP release.

Conclusions:

• TRPV2 is expressed in the human airway epithelium.
• TRPV2 plays a role in modulating adenosine triphosphate release in response to mechanical stimulation.