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Blood, Vol. 105, Issue 3, 1127-1134, February 1, 2005
Gi-independent macrophage chemotaxis to lysophosphatidylcholine via the immunoregulatory GPCR G2A
Blood Yang et al.
105: 1127
Supplemental materials for: Yang et al, Vol 105, Issue 3, 1127-1134
Files in this Data Supplement:
- Figure S1. Gi signaling in LPC-G2A mediated chemotaxis of DO 11.10 and U937 cells (JPG, 48 KB)
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Cells were pretreated with 100 ng/mL pertussis toxin (PTX) or control buffer for 16 hours in a cell culture incubator at 37°C. Chemotaxis of these cells to LPC and SDF-1 was assessed in transwell plates with 5-µm pore size polycarbonate filters. For these suspension cells, cells migrating through filters dropped into lower chambers and were counted by an automatic cell counter (Beckman Coulter). (A, B) Effects of PTX on chemotaxis of wild-type and G2AHIGH DO11.10 mouse T-hybridoma cells to LPC and SDF-1. Migration of DO11.10 cells to LPC was enhanced by G2A overexpression and was resistant to PTX. Chemotaxis towards SDF-1 was used as a control that is sensitive to PTX. (C, D) Effects of PTX on chemotaxis of wild-type and G2AHIGH U937 human monoblastic cells to LPC and SDF-1α. Wild-type U937 cells did not migrate to LPC, since these cells do not express G2A or GPR4 (Yun et al). U937 cells overexpressing G2A were chemotactic to LPC, and the migration was insensitive to PTX. As a control, the chemotaxis of U937 cells to SDF-1 was abolished by PTX treatment. The results are representative of at least 2 independent experiments.
Yun MR, Okajima F, Im DS. Action mode of lysophosphatidylcholine in human monocytes. J Pharmacol Sci. 2004;94:45-50.
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