Endogenously expressed apoprotein e3 (apoe) has constrasting effects on cell lipid metabolism to exogenously derived apo e y Academic Article uri icon


MeSH Major

  • Fractures, Compression
  • Lumbar Vertebrae
  • Spinal Fractures
  • Thoracic Vertebrae


  • Exogenous apoE on model triglycéride rich particles (TGRP) increases triglyceride (TG) utilization and cholesterylecter (CE) hydrolysis independent of its effect on enhancing particle uptake. We questioned if endogenously expressed apoE had effects on TGRP metabolism similar to exogenous apoE. J774-A1 macrophage, which do not express apoE, were transfected with a apo£3 cDNA expression construct(E+) or control vector(E-). Fluorescence microscopy and immunoblots showed endogenous apoE in Golgi-like structures and secreted into media. In contrast, exogenously supplied apoE on TGRP targeted to endocytic compartments in both E+ and E- cells. To study the effects of apoE expression on lipid metabolism, cells were incubated for 4-611 with or without recombinant apoE on model IDL size TGRP, 50-1200/tg, neutral lipid/ml by sontcation of triolein: cbolesteryl oleate (1:1) with egg lecithin. Surprisingly, E- cells displayed 3-4 fold higher TGRP uptake than E + cells. Endogenous apoE expression does not affect TGRP uptake through LDL receptors(R), LDLR related proteins (LRP), class I or class II scavenger R's, but endogenous apoE may interfere with TGRP uptake by blocking TGRP binding to cell surfece beparin sulfate proteoglycans. 2-3 fold higher TG mass (relative to uptake), with no difference in TG synthesis implied 30-50% ICH TG utilization in E + vs E- cells. CE hydrolysis in E + cells was 25 % lower than E- cells. Adding exogenous apoE stimulated TGRP uptake, TG utilization, and CE hydrolysis in both cell lines. Thus, cell expressed apoE follows very différait intracellular pathways than does exogenous TGRP apoE, and this may explain their contrasting effects on TGRP catabolism and likely, other metabolic pathways. (NIH IHL40404).

publication date

  • December 1996



  • Academic Article

Additional Document Info

start page

  • A722


  • 10


  • 3