Lysophosphatidic acid signaling in airway epithelium: role in airway inflammation and remodeling.

摘要: Abstract Lysophosphatidic acid (LPA), a potent bioactive phospholipid, induces diverse cellular responses, including cell proliferation, migration, and cytokine release. LPA can be generated intracellularly extracellularly through multiple synthetic pathways by action of various enzymes, such as phospholipase A 1/2 (PLA ), D (PLD), acylglycerol kinase (AGK), lysophospholipase (lysoPLD). Metabolism is regulated family lipid phosphate phosphatases (LPPs). Significant amounts have been detected in biological fluids, serum, saliva, bronchoalveolar lavage fluid (BALF). The most significant effects appear to activation the G-protein-coupled receptors (GPCRs), termed 1–6 . regulates gene expression several transcriptional factors, nuclear factor-κB (NF-κB), AP-1, C/EBPβ. In addition GPCRs, cross-talk between receptor tyrosine kinases (RTKs) partly LPA-induced intracellular signaling responses. Airway epithelial cells participate innate immunity release cytokines, chemokines, mediators, other inflammatory mediators an increase barrier function response variety inhaled stimuli. Expression has demonstrated airway cells. This review summarizes our recent observations role LPA/LPA-Rs regulation epithelium, especially relation secretion pro- anti-inflammatory function.