2017年3月23日， 國際學術權威刊物自然出版集團旗下子刊《Scientific Reports》雜誌線上發表了清華大學生命科學學院杜力軍教授課題組題為“TRPM8 in the negative regulation of TNFα expression during cold stress”的研究論文， 論文第一作者是生命學院博士生王欣佩。
該文首次報告了作為胞內信號而不是膜受體的TRPM8、在冷應激條件下通過結合NFκB、進而抑制其轉位啟動起動TNFα轉錄表達、最終抑制炎性壞死因數的分子機制， 並由此發現了膜受體可以作為細胞內蛋白進行信號轉導的另一方面。 該工作的意義在於發現並闡明了局部低溫有助於抑制炎性反應的分子機制， 為臨床上創傷低溫冷敷療法提供了實驗依據。
TRPM8調控TNFα表達示意圖。
原文連結：
原文摘要：
Transient Receptor Potential Melastatin-8 (TRPM8) reportedly plays a fundamental role in a variety of processes including cold sensation, thermoregulation, pain transduction and tumorigenesis. However, the role of TRPM8 in inflammation under cold conditions is not well known. Since cooling allows the convergence of primary injury and injury-induced inflammation, we hypothesized that the mechanism of the protective effects of cooling might be related to TRPM8. We therefore investigated the involvement of TRPM8 activation in the regulation of inflammatory cytokines. The results showed that TRPM8 expression in the mouse hypothalamus was upregulated when the ambient temperature decreased; simultaneously, tumor necrosis factor-alpha (TNFα) was downregulated. The inhibitory effect of TRPM8 on TNFα was mediated by nuclear factor kappa B (NFκB). Specifically, cold stress stimulated the expression of TRPM8, which promoted the interaction of TRPM8 and NFκB, thereby suppressing NFκB nuclear localization. This suppression consequently led to the inhibition of TNFα gene transcription. The present data suggest a possible theoretical foundation for the anti-inflammatory role of TRPM8 activation, providing an experimental basis that could contribute to the advancement of cooling therapy for trauma patients.