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      Low- and High-Density Lipoproteins as Mitogenic Factors for Vascular Smooth Muscle Cells: Individual, Additive and Synergistic Effects

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          The mitogenic activities of low (LDL)- and high (HDL)-density lipoproteins have been examined in cultures of human vascular smooth muscle cells (VSMC). LDL and HDL<sub>3</sub> dose-dependently (EC50 values ∼50 µg/ml) stimulated DNA and protein synthesis ([<sup>3</sup>H]-thymidine and [<sup>3</sup>H]-leucine incorporation, respectively) in the absence of exogenously added mitogens. The synthetic responses of VSMC to combinations of LDL and HDL<sub>3</sub> were additive, indicating that each lipoprotein mediates discrete effects. LDL or HDL<sub>3</sub> promoted VSMC proliferation under strict mitogen-free conditions, but this growth response was not sustained. VSMC exposed to combinations of lipoproteins (either LDL or HDL<sub>3</sub>) and growth factors (either PDGF-BB, EGF, bFGF or IGF) exhibited synergistic DNA synthesis responses. In the combined presence of PDGF-BB and either LDL or HDL<sub>3</sub>, VSMC proliferation was sustained. Anionized lipoprotein preparations (oxidized, acetylated, carbamylated or malonimylated) also stimulated DNA and protein synthesis. Since the antioxidant β-ydroxylated toluene did not block the effect of native LDL on DNA synthesis, and fucoidin, a specific competitor for the ‘scavenger’ receptor, did not inhibit oxidized LDL-induced DNA synthesis, activation of mitogenic signals by lipoproteins does not depend on lipid peroxidation. Rather, the apparent intrinsic mitogenic potential of lipoproteins may depend upon their direct activation of replication-coupled signal transduction systems.

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          Author and article information

          J Vasc Res
          Journal of Vascular Research
          S. Karger AG
          24 September 2008
          : 32
          : 5
          : 328-338
          aDepartment of Research, University Hospital of Basel, Switzerland; bLaboratory of Molecular Endocrinology, Institute of Experimental Cardiology, Cardiology Research Center, Moscow, Russia
          159107 J Vasc Res 1995;32:328–338
          © 1995 S. Karger AG, Basel

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          Pages: 11
          Original Paper


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