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Stromal interaction molecules (STIM1, 2) are acting as sensors for Ca 2+  in intracellular stores and activate Orai channels at the plasma membrane for store-operated Ca 2+  entry (SOCE), while classical transient receptor potential (TRPC) channel mediate receptor-operated Ca 2+  entry (ROCE). Several reports, however, indicate a role for TRPC in SOCE in certain cell types. Here, we analyzed Ca 2+  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.

scientific reports

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