title: [Effect of Ox-LDL on cell cycling phases and PCNA, P53, P27 and c-erbB-2 expression in cultured human arterial smooth muscle cells].
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.
authors.affiliation: Apolipoprotein Research Unit, Institute of Biochemistry and Molecular Biology, Chengdu.
authors.forename: Z
authors.initials: Z
authors.lastname: Li
authors.forename: B
authors.initials: B
authors.lastname: Liu
authors.forename: Y
authors.initials: Y
authors.lastname: Wei
mesh_terms: D001011:Aorta / Q000166:cytology; D018797:Cell Cycle Proteins; D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D050760:Cyclin-Dependent Kinase Inhibitor p27; D005333:Fetus; D006801:Humans; D008077:Lipoproteins, LDL / Q000494:pharmacology*; D008869:Microtubule-Associated Proteins / Q000096:biosynthesis; D009131:Muscle, Smooth, Vascular / Q000166:cytology* / Q000378:metabolism; D010084:Oxidation-Reduction; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism*; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000096:biosynthesis; D016196:S Phase; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis; D025521:Tumor Suppressor Proteins
chemical_list: D018797:Cell Cycle Proteins; D050760:Cyclin-Dependent Kinase Inhibitor p27; D008077:Lipoproteins, LDL; D008869:Microtubule-Associated Proteins; D018809:Proliferating Cell Nuclear Antigen; D018719:Erb-b2 Receptor Tyrosine Kinases; D016159:Tumor Suppressor Protein p53; D025521:Tumor Suppressor Proteins; C099252:oxidized low density lipoprotein