TY - JOUR
T1 - The effect of three serum basic proteins on the mass of lipids in normal and hyperapoB fibroblasts
AU - Kwiterovich, Peter O.
AU - Motevalli, Mahnaz
AU - Miller, Michael
PY - 1994
Y1 - 1994
N2 - We studied whether serum basic proteins (BPs) produce abnormal changes in the mass of cellular lipids in fibroblasts from patients with hyperapobetalipoproteinemia (hyperapoB) and if inhibition or stimulation of protein kinase C affects these processes. In normal cells, BP I increased the mean mass of triglycerides about twofold, whereas there was significantly less stimulation in hyperapoB cells (P<.005). The increase in the mass of cell cholesteryl esters seen in normal cells with BP I was also significantly reduced in hyperapoB cells (P<.005). In contrast, BP II abnormally stimulated the mass of cell cholesteryl esters sixfold in hyperapoB cells (P<.005). BP I also stimulated the mass of total phospholipids about twofold in normal cells, an effect that was reduced by about one third in hyperapoB cells (P=.08). No abnormality was found in hyperapoB cells with BP III. H-7, an inhibitor of protein kinase C, decreased the effects of BP I and BP II in normal and hyperapoB cells. C:8, an analogue of diacylglycerol, activated protein kinase C and stimulated triglyceride formation in normal (fourfold) and hyperapoB (fivefold) cells in the absence of BP I. When added with C:8, BP I further increased triglyceride production 1.5-fold in normal cells but not in hyperapoB cells. Two cellular abnormalities in lipid metabolism in hyperapoB fibroblasts were found, one with BP I, another with BP II. Protein kinase C activity was not deficient in hyperapoB cells, and the defect(s) may occur at another, perhaps earlier, step in the pathway.
AB - We studied whether serum basic proteins (BPs) produce abnormal changes in the mass of cellular lipids in fibroblasts from patients with hyperapobetalipoproteinemia (hyperapoB) and if inhibition or stimulation of protein kinase C affects these processes. In normal cells, BP I increased the mean mass of triglycerides about twofold, whereas there was significantly less stimulation in hyperapoB cells (P<.005). The increase in the mass of cell cholesteryl esters seen in normal cells with BP I was also significantly reduced in hyperapoB cells (P<.005). In contrast, BP II abnormally stimulated the mass of cell cholesteryl esters sixfold in hyperapoB cells (P<.005). BP I also stimulated the mass of total phospholipids about twofold in normal cells, an effect that was reduced by about one third in hyperapoB cells (P=.08). No abnormality was found in hyperapoB cells with BP III. H-7, an inhibitor of protein kinase C, decreased the effects of BP I and BP II in normal and hyperapoB cells. C:8, an analogue of diacylglycerol, activated protein kinase C and stimulated triglyceride formation in normal (fourfold) and hyperapoB (fivefold) cells in the absence of BP I. When added with C:8, BP I further increased triglyceride production 1.5-fold in normal cells but not in hyperapoB cells. Two cellular abnormalities in lipid metabolism in hyperapoB fibroblasts were found, one with BP I, another with BP II. Protein kinase C activity was not deficient in hyperapoB cells, and the defect(s) may occur at another, perhaps earlier, step in the pathway.
KW - Cholesterol
KW - Cholesteryl esters
KW - Free fatty acids
KW - Hyperlipidemia
KW - Phospholipids
KW - Protein kinase C
KW - Triglycerides
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U2 - 10.1161/01.ATV.14.1.1
DO - 10.1161/01.ATV.14.1.1
M3 - Article
C2 - 8274464
AN - SCOPUS:0028177455
SN - 1079-5642
VL - 14
SP - 1
EP - 7
JO - Arteriosclerosis, thrombosis, and vascular biology
JF - Arteriosclerosis, thrombosis, and vascular biology
IS - 1
ER -