Tumor Necrosis Factor-α Regulates the TRPA1 Expression in Human Odontoblast-Like Cells

Our study demonstrated that TRPA1 expression in HOD-like cells was evidently upregulated by TNF-α, presumably via TNFR1. TNF-α induced significant increasement in the intracellular distributions of TRPA1 proteins, with increases in the cytoplasm, ER membrane, and mitochondria, to actively participate in noxious external stimuli perception and transduction of hyperalgesia.

Immunohistochemistry was used to confirm the expression of TRPA1 channel in HODs. Dental pulp cells were induced and differentiated to HOD-like cells and used in succedent experiments. Real-time quantitative polymerase chain reaction assay and Western blotting were used to examine the expression changes of TRPA1 channel with the presence and absence of TNF-α and TNF receptor (TNFR) inhibitor, R 7050. Finally, immunoelectron microscopy (IEM) and quantitative analysis were performed to directly display the TNF-α-regulated distribution change of TRPA1 channel in HOD-like cells.

Transient receptor potential cation channel, subfamily A, member 1 (TRPA1) is a promiscuous chemical nociceptor involved in the perception of cold hypersensitivity, mechanical hyperalgesia and inflammatory pain in human odontoblasts (HODs). Here, we aimed to study the underlying mechanism in which inflammatory cytokine tumor necrosis factor (TNF)-α regulated the expression of TRPA1 channel at both cellular and subcellular levels. Materials and

TRPA1 channel was positively expressed in the cell bodies and processes of HODs. The expression TRPA1 channel was significantly up-regulated by high concentration of TNF-α, which could be suppressed by R 7050. Under IEM, TNF-α treatment could increase the expression of TRPA1 in the ER membrane, cytoplasm and mitochondria.