| First Author | Bendiks L | Year | 2020 |
| Journal | Sci Rep | Volume | 10 |
| Issue | 1 | Pages | 6812 |
| PubMed ID | 32321939 | Mgi Jnum | J:298507 |
| Mgi Id | MGI:6480195 | Doi | 10.1038/s41598-020-63677-2 |
| Citation | Bendiks L, et al. (2020) Store-operated Ca(2+) entry in primary murine lung fibroblasts is independent of classical transient receptor potential (TRPC) channels and contributes to cell migration. Sci Rep 10(1):6812 |
| abstractText | 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(DeltapmLF)) 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. |
