Roles of store-operated Ca channels in regulating cell cycling and migration of human cardiac c-kit progenitor cells

Che H, Li G, Sun HY, Xiao GS, Wang Y, Li GR. Roles of store-operated Ca channels in regulating cell cycling and migration of human cardiac c-kit progenitor cells. Am J Physiol Heart Circ Physiol 309: H1772–H1781, 2015. First published October 9, 2015; doi:10.1152/ajpheart.00260.2015.—Cardiac c-kit progenitor cells are important for maintaining cardiac homeostasis and can potentially contribute to myocardial repair. However, cellular physiology of human cardiac c-kit progenitor cells is not well understood. The present study investigates the functional store-operated Ca entry (SOCE) channels and the potential role in regulating cell cycling and migration using confocal microscopy, RT-PCR, Western blot, coimmunoprecipitation, cell proliferation, and migration assays. We found that SOCE channels mediated Ca influx, and TRPC1, STIM1, and Orai1 were involved in the formation of SOCE channels in human cardiac c-kit progenitor cells. Silencing TRPC1, STIM1, or Orai1 with the corresponding siRNA significantly reduced the Ca signaling through SOCE channels, decreased cell proliferation and migration, and reduced expression of cyclin D1, cyclin E, and/or p-Akt. Our results demonstrate the novel information that Ca signaling through SOCE channels regulates cell cycling and migration via activating cyclin D1, cyclin E, and/or p-Akt in human cardiac c-kit cells.