TRPA1 is essential for the vascular response to environmental cold exposure

Aisah A. Aubdool, Rabea Graepel, Xenia Kodji, Khadija M. Alawi, Jennifer V. Bodkin, Salil Srivastava, Clive Gentry, Richard Heads, Andrew D. Grant, Elizabeth S. Fernandes, Stuart Bevan and Susan D. Brain ()
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Aisah A. Aubdool: BHF Cardiovascular Centre of Excellence and Centre of Integrative Biomedicine, King’s College London
Rabea Graepel: BHF Cardiovascular Centre of Excellence and Centre of Integrative Biomedicine, King’s College London
Xenia Kodji: BHF Cardiovascular Centre of Excellence and Centre of Integrative Biomedicine, King’s College London
Khadija M. Alawi: BHF Cardiovascular Centre of Excellence and Centre of Integrative Biomedicine, King’s College London
Jennifer V. Bodkin: BHF Cardiovascular Centre of Excellence and Centre of Integrative Biomedicine, King’s College London
Salil Srivastava: BHF Cardiovascular Centre of Excellence and Centre of Integrative Biomedicine, King’s College London
Clive Gentry: Wolfson Centre for Age Related Diseases, King’s College London
Richard Heads: BHF Cardiovascular Centre of Excellence and Centre of Integrative Biomedicine, King’s College London
Andrew D. Grant: Wolfson Centre for Age Related Diseases, King’s College London
Elizabeth S. Fernandes: BHF Cardiovascular Centre of Excellence and Centre of Integrative Biomedicine, King’s College London
Stuart Bevan: Wolfson Centre for Age Related Diseases, King’s College London
Susan D. Brain: BHF Cardiovascular Centre of Excellence and Centre of Integrative Biomedicine, King’s College London

Nature Communications, 2014, vol. 5, issue 1, 1-13

Abstract: Abstract The cold-induced vascular response, consisting of vasoconstriction followed by vasodilatation, is critical for protecting the cutaneous tissues against cold injury. Whilst this physiological reflex response is historic knowledge, the mechanisms involved are unclear. Here by using a murine model of local environmental cold exposure, we show that TRPA1 acts as a primary vascular cold sensor, as determined through TRPA1 pharmacological antagonism or gene deletion. The initial cold-induced vasoconstriction is mediated via TRPA1-dependent superoxide production that stimulates α2C-adrenoceptors and Rho-kinase-mediated MLC phosphorylation, downstream of TRPA1 activation. The subsequent restorative blood flow component is also dependent on TRPA1 activation being mediated by sensory nerve-derived dilator neuropeptides CGRP and substance P, and also nNOS-derived NO. The results allow a new understanding of the importance of TRPA1 in cold exposure and provide impetus for further research into developing therapeutic agents aimed at the local protection of the skin in disease and adverse climates.

Date: 2014
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DOI: 10.1038/ncomms6732

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