Leukotriene B4 stimulation of phagocytes results in the formation of inositol 1,4,5-trisphosphate. A second messenger for Ca2+ mobilization.

摘要: Inositol trisphosphate (InsP3) production and cytosolic free Ca2+ ([Ca2+]i) elevations induced by leukotriene B4 (LTB4)-receptor activation were studied in the human promyelocytic-leukaemia cell line HL60, to differentiate retinoic acid. The myeloid-differentiated HL60 cells respond LTB4 raising their [Ca2+]i with a dose-response relationship similar that shown normal neutrophils. observations of transduction mechanism compared those chemotactic peptide fMet-Leu-Phe differentiated dimethyl sulphoxide. Both triggered rapid (less than 5 s) elevation [Ca2+]i, which occurred parallel InsP3 from myo-[3H]inositol-labelled cells. threshold concentrations agonists, for production, found at 10(-9) M, slightly higher concentration required detect elevations. No significant changes noted phosphoinositide levels upon stimulation LTB4. Exposure Bordetella pertussis toxin before abolished both increased formation rise [Ca2+]i. elicited inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] no detectable lag time, followed slower more sustained 1,3,4-trisphosphate Stimulation various analogues revealed good correlation between total as well Ins(1,4,5)P3 [Ca2+]1. Thus receptor results an via also involving nucleotide regulatory protein, previously described mechanism.