ArticleAmerican journal of physiology. Cell physiology2010
Endothelial cells isolated from caveolin-2 knockout mice display higher proliferation rate and cell cycle progression relative to their wild-type counterparts.
Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- QAL333's antitumor activity and predictive modeling: integrated transcriptomic-bioinformatic analysis reveals selective cytotoxicity and sensitivity determinants.Scientific reports · 2026Article
- Downregulation of Caveolin-2 Is a Novel Mechanism Involved in Activation of Inducible Nitric Oxide Synthase (iNOS) in Mouse Peritoneal Macrophages.Mediators of inflammation · 2026Article
- Increased Caveolin-2 Expression in Brain Endothelial Cells Promotes Age-Related Neuroinflammation.Molecules and cells · 2022Article
- Identification of Estrogen Signaling in a Prioritization Study of Intraocular Pressure-Associated Genes.International journal of molecular sciences · 2021Article
- Critical Role of Caveolin-1 Loss/Dysfunction in Pulmonary Hypertension.Medical sciences (Basel, Switzerland) · 2021Review
- Elevated postischemic tissue injury and leukocyte-endothelial adhesive interactions in mice with global deficiency in caveolin-2: role of PAI-1.American journal of physiology. Heart and circulatory physiology · 2021Article
- Lung Endothelial Transcytosis.Comprehensive Physiology · 2020Review
- Caveolin-1 and Caveolin-2 Can Be Antagonistic Partners in Inflammation and Beyond.Frontiers in immunology · 2017Review
- Isolation and characterization of renal cancer stem cells from patient-derived xenografts.Oncotarget · 2016Article
- Deformation of the Outer Hair Cells and the Accumulation of Caveolin-2 in Connexin 26 Deficient Mice.PloS one · 2015Article
- Host deficiency in caveolin-2 inhibits lung carcinoma tumor growth by impairing tumor angiogenesis.Cancer research · 2014Article
- Cell proliferation in in vivo-like three-dimensional cell culture is regulated by sequestration of ERK1/2 to lipid rafts.Cell proliferation · 2014Article
- Adaptive response of vascular endothelial cells to an acute increase in shear stress frequency.American journal of physiology. Heart and circulatory physiology · 2013Article
- N-terminal tyrosine phosphorylation of caveolin-2 negates anti-proliferative effect of transforming growth factor beta in endothelial cells.FEBS letters · 2012Article
- Caveolae, caveolins, cavins, and endothelial cell function: new insights.Frontiers in physiology · 2012Article
- Caveolin-2 is a negative regulator of anti-proliferative function and signaling of transforming growth factor-β in endothelial cells.American journal of physiology. Cell physiology · 2011Article
- Lysophosphatidic Acid Stimulates the Proliferation of Ovarian Cancer Cells via the gep Proto-Oncogene Gα(12).Genes & cancer · 2011Article
- A novel domain of caveolin-2 that controls nuclear targeting: regulation of insulin-specific ERK activation and nuclear translocation by caveolin-2.Journal of cellular and molecular medicine · 2011Article
- Novel insights into the role of caveolin-2 in cell- and tissue-specific signaling and function.Biochemistry research international · 2011Article
- Regulation of Cell Signaling and Function by Endothelial Caveolins: Implications in Disease.Translational medicine (Sunnyvale, Calif.)Article
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Authors and funding
4 authors.
Funding
Abstract
The goal of this study was to determine whether caveolin-2 (Cav-2) is capable of controlling endothelial cell (EC) proliferation in vitro. To realize this goal, we have directly compared proliferation rates and cell cycle-associated signaling proteins between lung ECs isolated from wild-type (WT) and Cav-2 knockout (KO) mice. Using three independent proliferation assays, we have determined that Cav-2 KO ECs proliferate by ca. 2-fold faster than their WT counterparts. Cell cycle analysis by flow cytometry of propidium iodide-stained cells showed a relatively higher percentage of Cav-2 KO ECs in S and G(2)/M and lower percentage in G(o)/G(1) phases of cell cycle relative to their WT counterparts. Furthermore, an over 2-fold increase in the percentage of S phase-associated Cav-2 KO relative to WT ECs was independently determined with bromodeoxyuridine incorporation assay. Mechanistically, the increase in proliferation/cell cycle progression of Cav-2 KO ECs correlated well with elevated expression levels of predominantly S phase- and G(2)/M phase-associated cyclin A and B1, respectively. Further mechanistic analysis of molecular events controlling cell cycle progression revealed increased level of hyperphosphorylated (inactive) form of G(1) to S phase transition inhibitor, the retinoblastoma protein in hyperproliferating Cav-2 KO ECs. Conversely, the expression level of the two cyclin-dependent kinase inhibitors p16(INK4) and p27(Kip1) was reduced in Cav-2 KO ECs. Finally, increased phosphorylation (activation) of proproliferative extracellular signal-regulated kinase 1/2 was observed in hyperproliferating Cav-2 KO ECs. Overall, our data suggest that Cav-2 negatively regulates lung EC proliferation and cell cycle progression.
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