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Gobeil, F. et al.

Gobeil, Bernier, Vazquez-Tello, Brault, Beauchamp, Quiniou, Marrache, Checchin, Sennlaub, Hou, Nader, Bkaily, Ribeiro-da-Silva, Goetzl, Chemtob,

Modulation of pro-inflammatory gene expression by nuclear lysophosphatidic acid receptor type-1.

Lysophosphatidic acid (LPA) is a bioactive molecule involved in inflammation, immunity, wound healing, and neoplasia. Its pleiotropic actions arise presumably by interaction with their cell surface G protein-coupled receptors. Herein, the presence of the specific nuclear lysophosphatidic acid receptor-1 (LPA1R) was revealed in unstimulated porcine cerebral microvascular endothelial cells (pCMVECs), LPA1R stably transfected HTC4 rat hepatoma cells, and rat liver tissue using complementary approaches, including radioligand binding experiments, electron- and cryomicroscopy, cell fractionation, and immunoblotting with three distinct antibodies. Coimmunoprecipitation studies in enriched plasmalemmal fractions of unstimulated pCMVEC showed that LPA1Rs are dually sequestrated in caveolin-1 and clathrin subcompartments, whereas in nuclear fractions LPA1R appeared primarily in caveolae. Immunofluorescent assays using a cell-free isolated nuclear system confirmed LPA1R and caveolin-1 co-localization. In pCMVEC, LPA-stimulated increases in cyclooxygenase-2 and inducible nitric-oxide synthase RNA and protein expression were insensitive to caveolea-disrupting agents but sensitive to LPA-generating phospholipase A2 enzyme and tyrosine kinase inhibitors. Moreover, LPA-induced increases in Ca2+ transients and/or iNOS expression in highly purified rat liver nuclei were prevented by pertussis toxin, phosphoinositide 3-kinase/Akt inhibitor wortmannin and Ca2+ chelator and channel blockers EGTA and SK&F96365, respectively. This study describes for the first time the nucleus as a potential organelle for LPA intracrine signaling in the regulation of pro-inflammatory gene expression.[1]

References

Modulation of pro-inflammatory gene expression by nuclear lysophosphatidic acid receptor type-1. Gobeil, F., Bernier, S.G., Vazquez-Tello, A., Brault, S., Beauchamp, M.H., Quiniou, C., Marrache, A.M., Checchin, D., Sennlaub, F., Hou, X., Nader, M., Bkaily, G., Ribeiro-da-Silva, A., Goetzl, E.J., Chemtob, S. J. Biol. Chem. (2003) [Pubmed]

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