Phospholipases in arterial tissue

Abstract

A B S T R A C T The role of phospholipases in the regulation of the changing phospholipid composition of normal human aortae with age was studied. Portions of grossly and histologically lesion-free ascending aortae from 16 females and 29 males obtained at autopsy, were analyzed for deoxyribonucleic acid (DNA), phospholipid, and cholesterol content and phospholipid composition. Enzymic activity toward four substrates, lecithin (LE), phosphatidyl ethanolamine, lysolecithin, and sphingomyelin (SP), was determined on portions of the same homogenate. By regression analysis for correlation between all determinations and age the following results were obtained: (a) total phospholipids and choleserol increased linearly with age; (b) the increase in sphingomyelin accounted for about 70% of the phospholipid increment; (c) hydrolysis of lecithin and phosphatidyl ethanolamine increased markedly with age, that of lysolecithin only moderately; (d) hydrolysis of sphingomyelin decreased with age; and (e) an inverse relation between the SP/LE ratio and age and sphingomyelinase/lecithinase activity and age was obtained. These results were interpreted to indicate that a causal relation exists between the fall in sphingomyelinase activity, both absolute and relative to lecithinase activity, and the accumulation of sphingomyelin with age.

Factors Determining the Concentrations of Lysolecithin in Plasma and Tissues

“…In vitro studies showed that the net uptake (Table V) of lysolecithin by atherosclerotic intima plus inner media was greater than that in control tissue, When no lysolecithin was added to the incubation medium, the quantity of ly- (2,11,16). The presence of albumin or other plasma proteins in the incubation medium containing lysolecithin greatly inhibited the rate of transfer of lysolecithin to the aorta (see also ref.…”

Sphingolipid Metabolism and Obesity-Induced Inflammation

“…LDL extracted from human atherosclerotic lesions has higher SM levels than LDL from plasma (Hoff and Morton, 1985; Guyton and Klemp, 1996; Schissel et al, 1996, 1998). A substantial amount of the SM found in arteries and atherosclerotic lesions appears to arise from SM synthesis in the arterial tissues (Zilversmit et al, 1961; Eisenberg et al, 1969). Plasma SM levels in atherogenic apoE KO mice are fourfold higher than in wild type mice (Jeong et al, 1998) and this may contribute to the increased atherosclerosis (Plump et al, 1992; Zhang et al, 1992).…”

Influence of Theobromine Magnesium Oleate on Formation of Experimental Atheroma

“…Since all the enzymes of the lipolytic pathway and the adenyl cyclase system are found in the arterial wall (17)(18)(19)(20)(21)(22)(23)(24)(25), it is possible that the site of action of TMO is in the arterial wall. However, the interrelation of the adenyl cyclase system and lipolysis has been more completely delineated in liver and adipose tissue and an action at these sites might also, indirectly, prevent lipid accumulation in arterial plaques.…”