The lipid molecule, lysophosphatidylinositol (LPI), is hypothesised to form part of a novel lipid signalling system that involves the G protein-coupled receptor GPR55 and distinct intracellular signalling cascades in endothelial cells. This work aimed to study the possible mechanisms involved in LPI-evoked cytosolic Ca2+ mobilization in human brain microvascular endothelial cells. Changes in intracellular Ca2+ concentrations were measured using cell population Ca2+ assay. LPI evoked biphasic elevation of intracellular calcium concentration, a rapid phase and a sustained phase. The rapid phase was attenuated by the inhibitor of PLC (U 73122), inhibitor of IP3 receptors, 2-APB and the depletor of endoplasmic reticulum Ca2+ store, thapsigargin. The sustained phase, on the other hand, was enhanced by U 73122 and abolished by the RhoA kinase inhibitor, Y-27632. In conclusion, the Ca2+ signal evoked by LPI is characterised by a rapid phase of Ca2+ release from the endoplasmic reticulum, and requires activation of the PLC-IP3 signalling pathway. The sustained phase mainly depends on RhoA kinase activation. LPI acts as novel lipid signalling molecule in endothelial cells, and elevation of cytosolic Ca2+ triggered by it may present an important intracellular message required in gene expression and controlling of vascular tone.
|Number of pages||10|
|Publication status||Published - 2016|
- RhoA kinase
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