Objective     

To explore the role of transient receptor potential melastatin 8 (TRPM8) receptor and related cold-induced signal transduction mechanism in airway epithelial cells.       Methods      The 16 HBE human airway epithelial cells were treated with cold temperature (18 ℃) and menthol. By means of Ca

2+

imaging

we explored the function of TRPM8 when the cells were pretreated with TRPM8 channel antagonist BCTC and exon-18-specific TRPM8 shRNA. Hydrolysis of phosphatidylinositol 4

5-bisphosphate (PIP2) were characterized by means of spatiotemporal dynamics of phospholipase C (PLC) δ1-pleckstrin homology-green fluorescent protein (δ1-PH-GFP).       Results      The concentration of intercellular calcium in the menthol and cold air treatment group (5.80±0.34

5.02±0.36)  higher than that in the control group (0.94±0.12) (P0.05). The intracellular calcium concentration was in the menthol+BCTC and menthol+TRPM8 shRNA groups (2.68±0.19

1.08±0.16)  than in the menthol treatment group (P0.05). The intracellular calcium concentration in the cold air + BCTC and cold air+TRPM8 shRNA groups (1.77±0.22

1.02±0.18) were lower than that in the cold air treatment group (P0.05). The translocation of PLC δ1-PH-GFP from the membrane to the cytosol (Fm/Fc) in the menthol treatment group and cold air treatment group (0.90±0.01

0.90±0.01) were higher than that in the control group (1.01±0.02) (P0.05). Fm/Fc was lower in the menthol+BCTC group and TRPM8 shRNA+menthol group (0.86±0.03

0.89±0.02) than in the menthol treatment group (P0.05)

and also lower in the cold air+BCTC group and cold air+TRPM8 shRNA group (0.82±0.02

0.93±0.01) than in the cold air treatment group (P0.05).       Conclusion      TRPM8 receptor is involved in the response to cold temperature in airway epithelial cells

and contributes to mucus hypersecretion through the TRPM8→Ca

2+

→ PLC→PIP2 signaling pathway.