[Diagnostic value of determination of the levels of phospholipase A2 in plasma lipoproteins and functional relations with C-reactive protein].
Laser correlation spectroscopy has indicated that plasma C-reactive protein (CRP) is present as a monomer and a pentamer (pentraxin); the latter is similar in physicochemical properties to apolipoproteins, the proteins that transfer fatty acids as nonpolar triglycerides to the cells in the intercellular medium. Concurrently, sepharose column chromatography revealed an association of the bulk of plasma CRP with very low-density lipoproteins. In parallel with CRP, the content of secretory phospholipase A, as a component of lipoproteins is on the rise; the enzyme hydrolyzes phosphatidylcholine in the surface monolayer of lipoproteins to form lysophosphatidylcholine that the CRP-pentamere displays a high affinity binding to. Two different immunochemical assays for CRP suggest that the CRP-monomere and the CRP-pentamere show different functional activity: the CRP-monomere is a humoral immunomodulator while the CRP-pentamere also activates interstitial tissue cells, but differently, by enhancing their energy provision with substrates, namely with saturated and unsaturated fatty acids as triglycerides as components of very low-density lipoproteins via CRP/apoB-100-receptor endocytosis. The vector ligand redirects the flow offatty acids towards the cells that directly show a biological inflammatory response. For this, lipoprotein-associated phospholipase A, hydrolyzes phosphatidylcholine to produce lysophosphatidylcholine that the CRP-pentamere binds to; it superimposes a physiological apoE/B-100-ligand, becomes itself a pathophysiological CRP/B-100-ligand, and directs a flow of the energy substrates towards the interstitial cells that exhibit pathophysiological CRB/B-100-receptors on the membrane. In the arterial intima, the functionally triglyceride-overloaded resident macrophages form lipid spots that form in each systemic inflammatory response or with the elevated plasma levels of a CRP-pentamere and phospholipase A, and are directly unrelated to atheromatosis. It seems likely that we have identified a monomer with the low plasma values of CRP and its bulk (this is a pentamere) with its high plasma values.
Titov
V N
VN
D000682:Amyloid / Q000378:metabolism; D000818:Animals; D002097:C-Reactive Protein / Q000032:analysis* / Q000737:chemistry / Q000378:metabolism / Q000502:physiology; D002318:Cardiovascular Diseases / Q000097:blood* / Q000201:enzymology / Q000517:prevention & control; D004730:Endothelium, Vascular / Q000201:enzymology / Q000378:metabolism; D006801:Humans; D008024:Ligands; D008074:Lipoproteins / Q000737:chemistry* / Q000378:metabolism; D015394:Molecular Structure; D064801:Phospholipase A2 Inhibitors; D054467:Phospholipases A2 / Q000097:blood* / Q000737:chemistry / Q000378:metabolism / Q000502:physiology; D011237:Predictive Value of Tests; D011485:Protein Binding
D000682:Amyloid; D008024:Ligands; D008074:Lipoproteins; D064801:Phospholipase A2 Inhibitors; D002097:C-Reactive Protein; D054467:Phospholipases A2