Abstract
Intracellular calcium (Ca 2+) homeostasis is very strictly regulated, and the activation of G-protein-coupled receptor (GPCR) can cause two different calcium changes, intracellular calcium release, and calcium influx. In this study, we investigated the possible role of lysophosphatidic acid (LPA) on GPCR-induced Ca 2+ signaling. The addition of exogenous LPA induced dramatic Ca 2+ influx but not intracellular Ca 2+ release in U937 cells. LPA-induced Ca 2+ influx was not affected by pertussis toxin and phospholipase C inhibitor (U73122), ruling out the involvement of pertussis toxin-sensitive G-proteins, and phospholipase C. Stimulation of U937 cells with Trp-Lys-Tyr-Met-Val- d-Met (WKYMVm), which binds to formyl peptide receptor like 1, enhanced phospholipase A 2 and phospholipase D activation, indicating LPA formation. The inhibition of LPA synthesis by phospholipase A 2-specific inhibitor (MAFP) or n-butanol significantly inhibited WKYMVm-induced Ca 2+ influx, suggesting a crucial role for LPA in the process. Taken together, we suggest that LPA mediates WKYMVm-induced Ca 2+ influx.
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