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

ABSTRACT: 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

SUBMITTER: Bendiks L 

PROVIDER: S-EPMC7176639 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature