ArticleMolecular and cellular biology1999
Confluence of vascular endothelial cells induces cell cycle exit by inhibiting p42/p44 mitogen-activated protein kinase activity.
Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 109 citations in OpenAlex.
- G0 or no-G0: phosphatase control of quiescence and cell cycle entry.Biochemical Society transactions · 2026Review
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- Same same but different? How blood and lymphatic vessels induce cell contact inhibition.Biochemical Society transactions · 2025Review
- Matrix Stiffness-Mediated DNA Methylation in Endothelial Cells.Cellular and molecular bioengineering · 2025Article
- IntracellularFrontiers in cellular and infection microbiology · 2025Article
- VEGF Induces Expression of Genes That Either Promote or Limit Relaxation of the Retinal Endothelial Barrier.International journal of molecular sciences · 2023Article
- Mathematical modelling of oxygen transport in a muscle-on-chip device.Interface focus · 2022Article
- Multi-omics study identifies novel signatures of DNA/RNA, amino acid, peptide, and lipid metabolism by simulated diabetes on coronary endothelial cells.Scientific reports · 2022Article
- Article
- Molecular control of cell density-mediated exit to quiescence.Cell reports · 2021Article
- Review
- Fluorescence-Based Nanoparticle Tracking Analysis and Flow Cytometry for Characterization of Endothelial Extracellular Vesicle Release.International journal of molecular sciences · 2020Article
- Interplay between thyroid cancer cells and macrophages: effects on IL-32 mediated cell death and thyroid cancer cell migration.Cellular oncology (Dordrecht, Netherlands) · 2019Article
- Analysis of biological networks in the endothelium with biomimetic microsystem platform.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Three-Layered Silk Fibroin Tubular Scaffold for the Repair and Regeneration of Small Caliber Blood Vessels: From Design toFrontiers in bioengineering and biotechnology · 2019Article
- Acid Sphingomyelinase Promotes Endothelial Stress Response in Systemic Inflammation and Sepsis.Molecular medicine (Cambridge, Mass.) · 2016Article
- Static mechanical strain induces capillary endothelial cell cycle re-entry and sprouting.Physical biology · 2016Article
- Cell Density-Dependent Increase in Tyrosine-Monophosphorylated ERK2 in MDCK Cells Expressing Active Ras or Raf.PloS one · 2016Article
- The Cell Adhesion Molecule Necl-4/CADM4 Serves as a Novel Regulator for Contact Inhibition of Cell Movement and Proliferation.PloS one · 2015Article
- Serum can overcome contact inhibition in confluent human pulmonary artery smooth muscle cells.PloS one · 2013Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Like other cellular models, endothelial cells in cultures stop growing when they reach confluence, even in the presence of growth factors. In this work, we have studied the effect of cellular contact on the activation of p42/p44 mitogen-activated protein kinase (MAPK) by growth factors in mouse vascular endothelial cells. p42/p44 MAPK activation by fetal calf serum or fibroblast growth factor was restrained in confluent cells in comparison with the activity found in sparse cells. Consequently, the induction of c-fos, MAPK phosphatases 1 and 2 (MKP1/2), and cyclin D1 was also restrained in confluent cells. In contrast, the activation of Ras and MEK-1, two upstream activators of the p42/p44 MAPK cascade, was not impaired when cells attained confluence. Sodium orthovanadate, but not okadaic acid, restored p42/p44 MAPK activity in confluent cells. Moreover, lysates from confluent 1G11 cells more effectively inactivated a dually phosphorylated active p42 MAPK than lysates from sparse cells. These results, together with the fact that vanadate-sensitive phosphatase activity was higher in confluent cells, suggest that phosphatases play a role in the down-regulation of p42/p44 MAPK activity. Enforced long-term activation of p42/p44 MAPK by expression of the chimera DeltaRaf-1:ER, which activates the p42/p44 MAPK cascade at the level of Raf, enhanced the expression of MKP1/2 and cyclin D1 and, more importantly, restored the reentry of confluent cells into the cell cycle. Therefore, inhibition of p42/p44 MAPK activation by cell-cell contact is a critical step initiating cell cycle exit in vascular endothelial cells.
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