Lysophosphatidic acid (LPA) induces plasma exudation and histamine release in mice via LPA receptors.

@article{Hashimoto2006LysophosphatidicA,
  title={Lysophosphatidic acid (LPA) induces plasma exudation and histamine release in mice via LPA receptors.},
  author={Terumasa Hashimoto and Hisayuki Ohata and Kazuo Honda},
  journal={Journal of pharmacological sciences},
  year={2006},
  volume={100 1},
  pages={
          82-7
        }
}
Lysophosphatidic acid (LPA), the simplest of the water-soluble phospholipids, can evoke various biological responses. The present study examined the activity of LPA to induce plasma exudation and histamine release in mice. Plasma exudation was assessed by extravasation of Evans blue. Subcutaneous administration of LPA (1 - 100 microg/site) led to increased plasma exudation in the skin. The LPA-induced plasma exudation was inhibited by ketotifen, a histamine H1-receptor antagonist, and… Expand
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TLDR
It is suggested that LPA-induced histamine release may be attributable to calcium release from intracellular stores and that Rho-associated protein kinase participates in the extracellular calcium-independent process of LPA, an inhibitor of ROCK. Expand
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It is suggested that LPA-induced airway hyperresponsiveness is attributable to activation of the Rho/ROCK-mediated pathway via endothelial cell differentiation gene (EDG) receptors, probably EDG 7. Expand
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Findings suggest that LPA-induced ISRs are attributable to histamine- and substance-P-mediated pathways, and the Rho/ROCK-mediated pathway may be involved. Expand
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Cultured cord blood-derived human MCs express mRNA transcripts for all 4 known receptors for lysophosphatidic acid (LPA), an abundant serum-associated lipid growth factor that acts through LPA receptor and PPAR-gamma-dependent pathways to accelerate hMC proliferation and differentiation, and it modulates their phenotype without providing cytoprotection. Expand
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Subtype-Selective Antagonists of Lysophosphatidic Acid Receptors Inhibit Platelet Activation Triggered by the Lipid Core of Atherosclerotic Plaques
TLDR
LPA molecules present in the core region of atherosclerotic plaques trigger rapid platelet activation through the stimulation of LPA1 and LPA3 receptors, and antagonists of platelet LPA receptors might provide a new strategy to prevent thrombus formation in patients with cardiovascular diseases. Expand
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TLDR
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TLDR
It is reported that dioctylglycerol pyrophosphate and dIOctylphosphatidic acid are selective antagonists of the LPA(1) and L PA(3) receptors, but prefer LPA (3) by an order of magnitude. Expand
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TLDR
Findings suggest that the LPA-induced nociception is attributed to the mechanism through vzg-1 receptor on nocICEptor endings, and to that through unidentified L PA-receptor on peripheral, possibly mast cells. Expand
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