Lipoprotein lipase increased low density lipoprotein retention by the subendothelial cell matrix more than fourfold without altering LDL transport across the monolayers.
Lipoprotein lipase markedly increases the retention of LDL and VLDL by the subendothelial matrix, providing a potential mechanism for atherogenic lipoprotein trapping in the arterial wall.
Effect estimate: more than fourfold increase
Lipoprotein lipase (LPL), the rate-limiting enzyme for hydrolysis of plasma lipoprotein triglycerides, is a normal constituent of the arterial wall. We explored whether LPL affects (a) lipoprotein transport across bovine aortic endothelial cells or (b) lipoprotein binding to subendothelial cell matrix (retention). When bovine milk LPL was added to endothelial cell monolayers before addition of 125I-labeled LDL, LDL transport across the monolayers was unchanged; but, at all concentrations of LDL tested (1-100 micrograms), LDL retention by the monolayers increased more than fourfold. 125I-labeled LDL binding to extracellular matrix increased when LPL was added directly to the matrix or was added to the basolateral side of the endothelial cell monolayers. Increased LDL binding required the presence of LPL and was not associated with LDL aggregation. LPL also increased VLDL, but not HDL, retention. Monoclonal anti-LPL IgG decreased both VLDL and LDL retention in the presence of LPL. Lipoprotein transport across the monolayers increased during hydrolysis of VLDL triglyceride (TG). In the presence of LPL and VLDL, VLDL transport across the monolayers increased 18% and LDL transport increased 37%. High molar concentrations of oleic acid to bovine serum albumin (3:1) in the medium increased VLDL transport approximately 30%. LDL transport increased 42% when oleic acid was added to the media. Therefore, LPL primarily increased retention of LDL and VLDL. A less remarkable increase in lipoprotein transport was found during hydrolysis of TG-containing lipoproteins. We hypothesize that LPL-mediated VLDL and LDL retention within the arterial wall potentiates conversion of these lipoproteins to more atherogenic forms.
Saxena et al. (Sat,) conducted a other in Atherosclerosis (in vitro model). Lipoprotein lipase (LPL) vs. Control (no LPL) was evaluated on LDL retention by subendothelial cell matrix (more than fourfold increase). Lipoprotein lipase increased low density lipoprotein retention by the subendothelial cell matrix more than fourfold without altering LDL transport across the monolayers.