Abstract
Several studies have shown lipoprotein lipase (LPL) activity in human placenta, but the quantitative significance and cellular specificity of LPL in this organ are unknown. The objective of this report is to investigate the metabolism of very-low-density lipoprotein triglycerides (VLDL-TG) by the placenta, the role of LPL in this process, and the types of cells involved. Placental cells were obtained by enzymatic digestion (collagenase, hyaluronidase, and DNA-ase) and separated on a 40% Percoll gradient. The trophoblasts were the predominant cell type (80% to 85% pure) isolated at d = 1.033 to 1.048 and macrophages were predominant at d = 1.077 to 1.100 (>95% pure), as characterized by eight immunocytochemical assays using cell protein-specific monoclonal antibodies. Macrophages represented 50% to 60% of cells isolated, and trophoblasts, 40% to 50%. LPL activity was assessed by VLDL-TG hydrolysis in primary 3- to 4-day tissue culture. In a representative experiment, LPL activity (nmol fatty acids (FA)/mg protein/24h) was 101.3 ± 5.3 in macrophages and 29.9 ± 6.5 in the predominant trophoblast cell types, with approximately 20% of these amounts incorporated and reesterified. VLDL-TG hydrolysis and cell lipid uptake in both placental cell types was essentially abolished by a monoclonal anti-LPL antibody. When compared with a model of hepatocytes (Hep G2 cells), the hydrolysis of VLDL-TG was almost undetectable in these cells. In contrast, free fatty acids (FFA) uptake by Hep G2 cells was fourfold to sixfold greater than that by macrophages and trophoblasts, respectively. In conclusion, macrophages and trophoblasts are the two predominant placental cells isolated by enzymatic digestion. The majority of VLDL-TG hydrolysis activity in tissue culture of placental cells arises from macrophages and is LPL-mediated. Compared with a cell model of hepatocyte function, VLDL-TGFA predominate as a source of FA for placental cells, while FFA predominate for the hepatocyte. Placental macrophages may play a role in the uptake of triglyceride-rich lipoprotein FA for placental storage, oxidation, and transfer to the fetus.
Published Version
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