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Modulation of voltage-dependent and inward rectifier potassium channels by 15-epi-lipoxin-a4 in activated murine macrophages: implications in innate immunity

AutorMoreno, Cristina; Prieto, Patricia ; Macías, Álvaro; Pimentel-Santillana, María ; Cruz, Alicia de la ; Través, Paqui G.; Boscá, Lisardo ; Valenzuela, Carmen
Fecha de publicación2013
EditorAmerican Association of Immunologists
CitaciónJournal of Immunology 191(12): 6136-6146 (2013)
ResumenPotassium channels modulate macrophage physiology. Blockade of voltage-dependent potassium channels (Kv) by specific antagonists decreases macrophage cytokine production and inhibits proliferation. In the presence of aspirin, acetylated cyclooxygenase-2 loses the activity required to synthesize PGs but maintains the oxygenase activity to produce 15R-HETE from arachidonate. This intermediate product is transformed via 5-LOX into epimeric lipoxins, termed 15-epi-lipoxins (15-epi-lipoxin A4 [e-LXA4]). Kv have been proposed as anti-inflammatory targets. Therefore, we studied the effects of e-LXA4 on signaling and on Kv and inward rectifier potassium channels (Kir) in mice bone marrow-derived macrophages (BMDM). Electrophysiological recordings were performed in these cells by the whole-cell patch-clamp technique. Treatment of BMDM with e-LXA4 inhibited LPS-dependent activation of NF-κB and IκB kinase ß activity, protected against LPS activation-dependent apoptosis, and enhanced the accumulation of the Nrf-2 transcription factor. Moreover, treatment of LPS-stimulated BMDM with e-LXA4 resulted in a rapid decrease of Kv currents, compatible with attenuation of the inflammatory response. Long-term treatment of LPS-stimulated BMDM with e-LXA4 significantly reverted LPS effects on Kv and Kir currents. Under these conditions, e-LXA4 decreased the calcium influx versus that observed in LPS-stimulated BMDM. These effects were partially mediated via the lipoxin receptor (ALX), because they were significantly reverted by a selective ALX receptor antagonist. We provide evidence for a new mechanism by which e-LXA4 contributes to inflammation resolution, consisting of the reversion of LPS effects on Kv and Kir currents in macrophages.
URIhttp://hdl.handle.net/10261/124016
DOI10.4049/jimmunol.1300235
Identificadoresdoi: 10.4049/jimmunol.1300235
issn: 0022-1767
e-issn: 1550-6606
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