Cold exposure lowers energy expenditure at the cellular level. (2nd April 2013)

• Record Type: Journal Article
• Authors: Park, Seyeon; Chun, Sohyun; Kim, Danuh
• Is Part Of: Cell biology international. Volume 37:Number 6(2013)
• Page Start: 638
• Page End: 642
• Publication Date: 2013-04-02
• Subjects: Cytology -- Periodicals; Cells -- Periodicals; 571.605
• DOI: 10.1002/cbin.10086
• Languages: English
• ISSNs: 1065-6995

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>Abstract</title> <sec id="cbin10086-sec-0001" sec-type="section"> <p>Mitochondrial function is intimately involved in various metabolic processes and is therefore essential to maintain cell viability. Of particular importance is the fact that mitochondrial membrane potential (ΔΨ<sub>m</sub>) is coupled with oxidative phosphorylation to drive adenosine triphosphate (ATP) synthesis. We have examined the effects of cold temperature stress on ΔΨ<sub>m</sub> and the role of cold temperature receptor expression on ΔΨ<sub>m</sub>. Human bronchial endothelial cell line, BEAS‐2B, and human embryonic kidney, HEK293, cell line were transfected with the gene for cold temperature responsive receptor protein TRPM8 or TRPA1, and exposed to cold temperature. ΔΨ<sub>m</sub> was monitored using 5, 5′, 6, 6′‐tetrachloro‐1, 1′, 3, 3′‐tetraethylbenzimidazoyl carbocyanine iodide derivative (JC‐10), a ΔΨ<sub>m</sub> probe. While cold temperatures significantly increased ΔΨ<sub>m</sub> and mitochondrial ATP levels in cells transfected with temperature responsive receptor TRPM8 or TRPA1, no change was noted in wild‐type cells. Moreover, the change in ΔΨ<sub>m</sub> and ATP level was a dynamic process. ΔΨ<sub>m</sub> was raised to peak levels within10 min of cold exposure, followed by a return to baseline levels at 30 min. Our findings suggest that cold temperature exposure increased mitochondrial ΔΨ<sub>m</sub> via a mechanism involving cold temperature receptors.</p> </sec> </abstract>