| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1949315 | Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids | 2013 | 7 Pages |
Lysophosphatidic acid (LPA), a simple bioactive phospholipid, is present in biological fluids such as plasma and bronchoalveolar lavage (BAL). It appears to have both pro- and anti-inflammatory roles in inflammatory lung diseases. Exogenous LPA promotes inflammatory responses by regulating the expression of chemokines, cytokines, and cytokine receptors in lung epithelial cells. In addition to the modulation of inflammatory responses, LPA regulates cytoskeleton rearrangement and confers protection against lung injury by enhancing lung epithelial cell barrier integrity and remodeling. The biological effects of LPA are mediated through its cell surface G-protein coupled LPA1–7 receptors. The roles of LPA receptors in lung fibrosis, asthma, and acute lung injury have been investigated using genetically engineered LPA receptor deficient mice and there appears to be a definitive role for endogenous LPA and its receptors in the pathogenesis of pulmonary inflammatory diseases. This review summarizes recent reports on the role of LPA and its receptors in the regulation of lung epithelial inflammatory responses and remodeling. This article is part of a Special Issue entitled: Advances in Lysophospholipid Research.
► LPA regulates cytokines and cytokine decoy receptors release in lung epithelial cells. ► LPA regulates cell–cell adherens junction and cell motility. ► LPA induces its biological responses via LPA receptors and intracellular signaling pathways. ► LPA receptors contribute to pathogenesis of lung inflammatory diseases.
