Store-operated Ca²⁺ entry in primary murine lung fibroblasts is independent of classical transient receptor potential (TRPC) channels and contributes to cell migration.

Stromal interaction molecules (STIM1, 2) are acting as sensors for Ca²⁺ in intracellular stores and activate Orai channels at the plasma membrane for store-operated Ca²⁺ entry (SOCE), while classical transient receptor potential (TRPC) channel mediate receptor-operated Ca²⁺ entry (ROCE). Several reports, however, indicate a role for TRPC in SOCE in certain cell types. Here, we analyzed Ca²⁺ influx and cell function in TRPC1/6-deficient (TRPC1/6^-/-) and STIM1/2- deficient (STIM1/2^ΔpmLF) primary murine lung fibroblasts (pmLF). As expected, SOCE was decreased in STIM1/2- deficient pmLF and ROCE was decreased in TRPC1/6^-/- pmLF compared to control cells. By contrast, SOCE was not significantly different in TRPC1/6^-/- pmLF and ROCE was similar in STIM1/2-deficient pmLF compared to Wt cells. Most interestingly, cell proliferation, migration and nuclear localization of nuclear factor of activated T-cells (NFATc1 and c3) were decreased after ablation of STIM1/2 proteins in pmLF. In conclusion, TRPC1/6 channels are not involved in SOCE and STIM1/2 deficiency resulted in decreased cell proliferation and migration in pmLF.

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