Our recent study showed that bradykinin increases cell cycling progression and migration of human cardiac c-Kit progenitor cells by activating pAkt and pERK1/2 signals. This study investigated whether bradykinin-mediated Ca signalling participates in regulating cellular functions in cultured human cardiac c-Kit progenitor cells using laser scanning confocal microscopy and biochemical approaches. It was found that bradykinin increased cytosolic free Ca ( ) by triggering a transient Ca release from ER IP3Rs followed by sustained Ca influx through store-operated Ca entry (SOCE) channel. Blockade of B2 receptor with HOE140 or IP3Rs with araguspongin B or silencing IP3R3 with siRNA abolished both Ca release and Ca influx. It is interesting to note that the bradykinin-induced cell cycle progression and migration were not observed in cells with siRNA-silenced IP3R3 or the SOCE component TRPC1, Orai1 or STIM1. Also the bradykinin-induced increase in pAkt and pERK1/2 as well as cyclin D1 was reduced in these cells. These results demonstrate for the first time that bradykinin-mediated increase in free via ER-IP3R3 Ca release followed by Ca influx through SOCE channel plays a crucial role in regulating cell growth and migration via activating pAkt, pERK1/2 and cyclin D1 in human cardiac c-Kit progenitor cells.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6156395 | PMC |
| http://dx.doi.org/10.1111/jcmm.13706 | DOI Listing |
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