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A Simple and Inexpensive Method for Determining Cold Sensitivity and Adaptation in Mice
Published on: March 17, 2015
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TRPA1 is essential for the vascular response to environmental cold exposure
Aisah A Aubdool1, Rabea Graepel1, Xenia Kodji1
1BHF Cardiovascular Centre of Excellence and Centre of Integrative Biomedicine, Cardiovascular Division, King's College London, London SE1 9NH, UK.
Nature Communications
|December 16, 2014
Summary
Transient Receptor Potential Ankyrin 1 (TRPA1) acts as a key cold sensor in blood vessels. TRPA1 mediates both cold-induced vasoconstriction and subsequent vasodilation, crucial for skin protection.
Area of Science:
- Physiology
- Molecular Biology
- Dermatology
Background:
- The cold-induced vascular response is vital for preventing cold injury.
- The precise molecular mechanisms underlying this response remain largely unknown.
Purpose of the Study:
- To elucidate the mechanisms of the cold-induced vascular response.
- To identify the role of TRPA1 in sensing cold and mediating vascular changes.
Main Methods:
- Utilized a murine model of local environmental cold exposure.
- Employed TRPA1 pharmacological antagonism and gene deletion.
- Investigated downstream signaling pathways including superoxide production, adrenoceptor stimulation, and neuropeptide release.
Main Results:
- TRPA1 was identified as a primary vascular cold sensor.
- Cold-induced vasoconstriction is TRPA1-dependent, involving superoxide, α2C-adrenoceptors, and Rho-kinase.
- TRPA1 activation also mediates vasodilation via CGRP, substance P, and nNOS-derived NO.
Conclusions:
- TRPA1 plays a critical dual role in the vascular response to cold exposure.
- Understanding TRPA1's function offers potential for therapeutic strategies against cold-induced skin damage.
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