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Peripheral thermosensation is the perception of external temperature. A change in temperature (on the surface of the skin and other tissues) is detected by a family of temperature-sensitive ion channels called Transient Receptor Potential, or TRP, receptors. These receptors are located on free nerve endings. Those detecting cold temperatures are closer to the surface of the skin than the nerve endings detecting warmth. These thermoTRP channels, while temperature selective, have relatively...
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Isolation of Retinal Arterioles for Ex Vivo Cell Physiology Studies
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TRPM2 channel regulates endothelial barrier function.

Claudie M Hecquet1, Gias U Ahmmed, Asrar B Malik

  • 1Department of Pharmacology and Center for Lung and Vascular Biology, University of Illinois College of Medicine, Chicago, IL, 60612, USA checqu1@uic.edu

Advances in Experimental Medicine and Biology
|March 6, 2010
PubMed
Summary
This summary is machine-generated.

Oxidative stress increases lung vascular permeability. The TRPM2 channel, activated by oxidants, is crucial for this process and neutrophil infiltration, suggesting it as a therapeutic target.

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Area of Science:

  • Endothelial cell biology
  • Oxidative stress research
  • Ion channel function

Background:

  • Oxidative stress, driven by hydrogen peroxide (H2O2), elevates vascular permeability and contributes to lung diseases.
  • The transient receptor potential melastatin 2 (TRPM2) channel is an oxidant-sensitive cation channel present in the vascular endothelium.

Purpose of the Study:

  • To investigate the role of TRPM2 in oxidant-induced endothelial hyperpermeability and neutrophil extravasation.
  • To explore the involvement of protein kinase Calpha (PKCalpha) in regulating TRPM2 channel activity.

Main Methods:

  • Utilized cultured pulmonary artery endothelial cells.
  • Examined TRPM2's role in mediating calcium entry and permeability changes.
  • Assessed neutrophil activation and extravasation.
  • Investigated the colocalization and regulatory function of PKCalpha with TRPM2.

Main Results:

  • TRPM2 mediates oxidant-induced calcium entry and endothelial hyperpermeability in pulmonary artery endothelial cells.
  • Neutrophil activation-dependent increases in endothelial permeability and extravasation require TRPM2.
  • PKCalpha positively regulates calcium entry through the functional TRPM2 channel.

Conclusions:

  • Endothelial TRPM2 activation by neutrophilic oxidants and PKCalpha regulation are critical for increased lung microvessel permeability and neutrophil sequestration.
  • Targeting TRPM2 function in the endothelium offers a potential strategy to combat oxidative stress-related vascular dysfunction.