title: Transcriptional up-regulation of p27(Kip1) during contact-induced growth arrest in vascular endothelial cells.
abstract: By plating porcine aortic endothelial cells at two different densities and thereby inducing two different time courses of contact-induced growth arrest, the temporal correlation between p27(Kip1) expression and cell cycle progression was investigated. When the quiescent cells were replated, they synchronously entered S phase with a peak at 20 h in both cases, while the cells plated at 25 and 80% of confluent densities exited the cell cycle by 96 and 48 h, respectively. Nuclear p27(Kip1) disappeared when the cells reentered the cell cycle and then recovered when the cells exited the cell cycle. The change in p27(Kip1) was associated with a concomitant change in Kip1 mRNA. The p27(Kip1) degradation activity did not increase in the cells reentering the cell cycle, nor did it decrease in the cells exiting the cell cycle. The Kip1 mRNA stability decreased in the growing cells and increased in the cells exiting the cell cycle and at confluence. A nuclear run-on assay revealed a close correlation between the Kip1 transcriptional activity and the level of Kip1 mRNA. We conclude that the cell-cell contact up-regulated the Kip1 gene transcription and increased the Kip1 mRNA stability, which was related to the recovery of p27(Kip1) protein during contact-induced growth arrest in endothelial cells.
authors.affiliation: Division of Molecular Cardiology, Kyushu University, Fukuoka, 812-8582, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Hirano
authors.forename: K
authors.initials: K
authors.lastname: Hirano
authors.forename: J
authors.initials: J
authors.lastname: Nishimura
authors.forename: H
authors.initials: H
authors.lastname: Kanaide
mesh_terms: D000818:Animals; D001681:Biological Assay; D001973:Bromodeoxyuridine; D002448:Cell Adhesion / Q000235:genetics; D002450:Cell Communication / Q000235:genetics*; D018929:Cell Culture Techniques / Q000379:methods; D002453:Cell Cycle / Q000235:genetics*; D018797:Cell Cycle Proteins / Q000235:genetics / Q000378:metabolism* / Q000494:pharmacology; D002457:Cell Extracts / Q000032:analysis; D002478:Cells, Cultured; D050760:Cyclin-Dependent Kinase Inhibitor p27; D016213:Cyclins / Q000378:metabolism; D003598:Cytoskeletal Proteins / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005455:Fluorescent Antibody Technique; D012333:RNA, Messenger / Q000378:metabolism; D013552:Swine; D013997:Time Factors; D015534:Trans-Activators; D014158:Transcription, Genetic / Q000502:physiology*; D025521:Tumor Suppressor Proteins / Q000235:genetics / Q000378:metabolism* / Q000494:pharmacology; D015854:Up-Regulation / Q000235:genetics*; D051176:beta Catenin
chemical_list: D018797:Cell Cycle Proteins; D002457:Cell Extracts; D016213:Cyclins; D003598:Cytoskeletal Proteins; D004791:Enzyme Inhibitors; D012333:RNA, Messenger; D015534:Trans-Activators; D025521:Tumor Suppressor Proteins; D051176:beta Catenin; D050760:Cyclin-Dependent Kinase Inhibitor p27; D001973:Bromodeoxyuridine