[Effect of Ox-LDL on cell cycling phases and PCNA, P53, P27 and c-erbB-2 expression in cultured human arterial smooth muscle cells]

Hua Xi Yi Ke Da Xue Xue Bao. 1998 Dec;29(4):394-8.
[Article in Chinese]

Abstract

It was found in our previous study that oxidative modification LDL (Ox-LDL) could stimulate the proliferation of cultured human arterial smooth muscle cells (SMC). Yet, the mechanism responsible for the SMC proliferation induced by Ox-LDL is not clear. Proliferating cell nuclear antiger (PCNA), P53 and P27 are the key regulatory factors of cell replication. In order to observe the effects of Ox-LDL on cell cycling phase and PCNA, P53, P27 and c-erb B-2 expression in SMC, we used the flow cytometric method in the present study on the proliferation of cultured human SMC induced by Ox-LDL. The results showed a relation between the Ox-LDL mediated SMC proliferation and the cycling phase shifting. The relative number of S phase cells in the Ox-LDL group was higher than that of the control group (22.9% vs 15.7%). Ox-LDL mediated SMC proliferation was accompanied with the increasing expression of PCNA. The percentage of specific PCNA positive FITC cells in the Ox-LDL group was significantly higher than that of the control group (12.6% vs 6.5%). PMA, an activitor of protein kinase C (PKC), stimulated SMC proliferation and increased the PCNA exression in cultured SMC, while the PKC inhibitor, F109203X, significantly decreased the PCNA expression in SMC (PCNA positive cells 13.4% vs 0.4%). No changes were observed in the expression of P53, P27 and c-erb B-2 in the cultured proliferating SMC induced by Ox-LDL. In all, the results suggest that the OX-LDL mediated SMC proliferation is related to increasing S Phase Cells and involved in the PCNA expression which might undergo the PKC cellular signal transduction pathway.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aorta / cytology
  • Cell Cycle Proteins*
  • Cell Division / drug effects
  • Cells, Cultured
  • Cyclin-Dependent Kinase Inhibitor p27
  • Fetus
  • Humans
  • Lipoproteins, LDL / pharmacology*
  • Microtubule-Associated Proteins / biosynthesis
  • Muscle, Smooth, Vascular / cytology*
  • Muscle, Smooth, Vascular / metabolism
  • Oxidation-Reduction
  • Proliferating Cell Nuclear Antigen / metabolism*
  • Receptor, ErbB-2 / biosynthesis
  • S Phase
  • Tumor Suppressor Protein p53 / biosynthesis
  • Tumor Suppressor Proteins*

Substances

  • Cell Cycle Proteins
  • Lipoproteins, LDL
  • Microtubule-Associated Proteins
  • Proliferating Cell Nuclear Antigen
  • Tumor Suppressor Protein p53
  • Tumor Suppressor Proteins
  • oxidized low density lipoprotein
  • Cyclin-Dependent Kinase Inhibitor p27
  • Receptor, ErbB-2