As part of the innate immune system, polymorphnuclear granulocytes play a major role in the elimination of bacterial pathogens. Neutrophil granulocytes circulate in the blood until they are recruited to inflamed tissues. After their activation they are chemically attracted and transmigrate the endothelium into the affected tissue.

The mechanism of cell migration describes changes in morphology und adhesion of cells. Ca²⁺ channels play a major role in signal transduction and control of this machinery. In this context, mechanosensitive Ca²⁺ channels are of particular interest since they possibly represent the crucial coordinative link between the protrusion of the leading edge and the retraction of the rear part of the migrating cell. Possible candidates for such Ca²⁺ channels are TRPC1 and TRPC6, members of the Transient Receptor Potential (TRP) channel family.

We studied the impact of either TRPC1 or TRPC6 on fMLP-stimulated migration of murine neutrophils on fibronectin matrices with time-lapse videomicroscopy and intracellular Ca²⁺ measurements. The – putative mechanosensory – function of TRPC1 and TRPC6 in neutrophil migration was shown by employing GsMTx-4, a blocking peptide for mechanosensitive ion channels. GsMTx-4 increased the cell area of migrating neutrophils, but had no effect in TRPC1-/- cells. This suggests that TRPC1 might regulate cell volume and adhesiveness during migration of murine neutrophils. The stimulation of TRPC6 activity by application of OAG strongly increased the velocity and translocation of neutrophils. Thus, TRPC1 and TRPC6 channels might both be involved in fMLP-induced migration of murine neutrophils.