Characterization of calcium signals provoked by lysophosphatidylinositol in human microvascular endothelial cells

Title:

Characterization of calcium signals provoked by lysophosphatidylinositol in human microvascular endothelial cells

Creator:

Al Suleimani, Y. M. and Hiley, C. R.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:e23514b0-2026-4780-8217-1d8af89cd323
uuid:e23514b0-2026-4780-8217-1d8af89cd323
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, vápník, calcium, lysophosphatidylinositol, GPR55, PLC, RhoA kinase, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

The lipid molecule, lysophosphatidylinositol (LPI), is hypothesis ed to form part of a novel lipid signalling system that involves the G protein- coupled receptor GPR55 and distinct in tracellular signalling cascades in endothelial cells. This work aimed to study the possible mechanisms involved in LPI -evoked cytosolic Ca 2+ mobilization in human brain microvascular endothelial cells. Changes in intracellular Ca 2+ concentrations were meas ured using cell population Ca 2+ 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 IP 3 receptors, 2 -APB and the de pletor of endoplasmic reticulum Ca 2+ 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 Ca 2+ signal evoked by LPI is characterised by a rapid phase of Ca 2+ release from the endoplasmic reticulum, and requires activation of the PLC -IP 3 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 Ca 2+ triggered by it may present an important intracellular message required in gene expression and controlling of vascular tone., Y. M. Al Suleimani, C. R. Hiley., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2016 Volume:65 | Number:1

Harvested from:

CDK

Metadata only:

false