Abstract
The role of nuclear membrane phospholipids as targets of phospholipases resulting in the generation of nuclear signaling messengers has received attention. In the present study, we have exploited the utility of electrospray ionization mass spectrometry to determine the phospholipid content of nuclei isolated from perfused hearts. Rat heart nuclei contained choline glycerophospholipids composed of palmitoyl and stearoyl residues at the sn-1 position with oleoyl, linoleoyl, and arachidonoyl residues at the sn-2 position. Diacyl molecular species were the predominant molecular subclass in the choline glycerophospholipids, with the balance of the molecular species being plasmalogens. In the ethanolamine glycerophospholipid pool from rat heart nuclei approximately 50% of the molecular species were plasmalogens, which were enriched with arachidonic acid at the sn-2 position. A 50% loss of myocytic nuclear choline and ethanolamine glycerophospholipids was observed in hearts rendered globally ischemic for 15 min followed by 90 min of reperfusion in comparisons with the content of these phospholipids in control perfused hearts. The loss of nuclear choline and ethanolamine glycerophospholipids during reperfusion of ischemic myocardium was partially reversed by the calcium-independent phospholipase A2 (iPLA2) inhibitor bromoenol lactone (BEL), suggesting that the loss of nuclear phospholipids during ischemia/reperfusion is mediated, in part, by iPLA2. Western blot analyses of isolated nuclei from ischemic hearts demonstrated that iPLA2 is translocated to the nucleus after myocardial ischemia. Taken together, these studies have demonstrated that nuclear phospholipid mass decreases after myocardial ischemia by a mechanism that involves, at least in part, phospholipolysis mediated by iPLA2.—Williams, S. D., F-F. Hsu, and D. A. Ford. Electrospray ionization mass spectrometry analyses of nuclear membrane phospholipid loss after reperfusion of ischemic myocardium. J. Lipid Res. 2000. 41: 1585–1595.
Highlights
The role of nuclear membrane phospholipids as targets of phospholipases resulting in the generation of nuclear signaling messengers has received attention
Ischemia/reperfusion-induced alterations in the mass of nuclear choline glycerophospholipid molecular species mediated by independent phospholipase A2 (iPLA2)
Analyses of nuclei isolated from control perfused rat myocardium by electrospray ionization mass spectrometry (ESI-MS) in the positive-ion mode demonstrated the preponderance of phosphatidylcholine molecular species predominantly containing either palmitic or stearic acids at the sn-1 position and either oleic, linoleic, or arachidonic acids at the sn-2 position [peaks at m/z 734 (16:0–16:0 phosphatidylcholine), 758 (16:0–18:2 phosphatidylcholine), 760 (16:0–18:1 phosphatidylcholine), 782 (16:0–20:4 phosphatidylcholine), 784 (18:1–18:2 phosphatidylcholine), 786 (18:0–18:2 phosphatidylcholine), 788 (18:0–18:1 phosphatidylcholine), 806 (16:0–22:6 phosphatidylcholine), 808 (18:1–20:4 phosphatidylcholine), 810 (18:0–20:4 phosphatidylcholine), and 834 (18:0–22:6 phosphatidylcholine)] (Fig. 1A and Table 1)
Summary
The role of nuclear membrane phospholipids as targets of phospholipases resulting in the generation of nuclear signaling messengers has received attention. Western blot analyses of isolated nuclei from ischemic hearts demonstrated that iPLA2 is translocated to the nucleus after myocardial ischemia. Taken together, these studies have demonstrated that nuclear phospholipid mass decreases after myocardial ischemia by a mechanism that involves, at least in part, phospholipolysis mediated by iPLA2.— Williams, S. In the current study, the unparalleled sensitivity of electrospray ionization mass spectrometry (ESI-MS) was exploited to characterize nuclear choline and ethanolamine glycerophospholipid molecular species and to determine the possible involvement of iPLA2 in nuclear phospholipid degradation. The loss of nuclear choline and ethanolamine glycerophospholipids after ischemia and reperfusion is, at least in part, mediated by iPLA2, which is translocated to the nucleus during myocardial ischemia
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