ArticleDevelopment (Cambridge, England)2015
Cdc42 is required for cytoskeletal support of endothelial cell adhesion during blood vessel formation in mice.
Article in Development (Cambridge, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
74 citing papers in PubMed, 108 citations in OpenAlex.
- Plasma Regulates Homeostatic Pulmonary Endothelial Signaling to Mitigate Vascular Leak Following Polytrauma and Hemorrhagic Shock.Shock (Augusta, Ga.) · 2026Article
- Prognostic Significance of Cdc42 Expression in Colorectal Cancer and Its Concordance Between Primary Tumors and Matched Metastases: A Retrospective Observational Study.Journal of clinical medicine · 2026Article
- Selective Targeting of Tip Endothelial Cells as a Therapeutic Strategy for Tumor Angiogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting Cdc42: Novel Approaches in Cardiovascular Disorders.Current protein & peptide science · 2026Review
- Lats1/2 Are Essential for Developmental Vascular Remodeling and Biomechanical Adaptation to Shear Stress.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Simulated Microgravity-Induced Alterations in PDAC Cells: A Potential Role for Trichostatin A in Restoring Cellular Phenotype.International journal of molecular sciences · 2025Article
- Cell communication and relevant signaling pathways in osteogenesis-angiogenesis coupling.Bone research · 2025Review
- Focal adhesion in the tumour metastasis: from molecular mechanisms to therapeutic targets.Biomarker research · 2025Review
- Antenatal phenotype associated with PAK2 pathogenic variants: bilateral pleural effusion as a warning sign.BMC medical genomics · 2025Article
- Endothelial tip-cell position, filopodia formation and biomechanics require BMPR2 expression and signaling.Communications biology · 2025Article
- Article
- Mechanisms of pulmonary endothelial barrier dysfunction in acute lung injury and acute respiratory distress syndrome.Chinese medical journal pulmonary and critical care medicine · 2024Article
- SH2 domain protein E and ABL signaling regulate blood vessel size.PLoS genetics · 2024Article
- Arf6 is required for endocytosis and filamentous actin assembly during angiogenesis in vitro.Microcirculation (New York, N.Y. : 1994) · 2023Article
- Age-Associated Changes in Endothelial Transcriptome and Epigenetic Landscapes Correlate With Elevated Risk of Cerebral Microbleeds.Journal of the American Heart Association · 2023Article
- Oscillatory shear stress-induced downregulation of TET1s injures vascular endothelial planar cell polarity by suppression of actin polymerization.APL bioengineering · 2023Article
- Endothelial-Specific Targeting of RhoA Signaling via CD31 Antibody-Conjugated Nanoparticles.The Journal of pharmacology and experimental therapeutics · 2023Article
- Identification of a physiologic vasculogenic fibroblast state to achieve tissue repair.Nature communications · 2023Article
- Arf6 Regulates Endocytosis and Angiogenesis by Promoting Filamentous Actin Assembly.bioRxiv : the preprint server for biology · 2023Article
- Actin cytoskeleton in angiogenesis.Biology open · 2022Review
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 5 institutions in 1 country.
Funding
Abstract
The Rho family of small GTPases has been shown to be required in endothelial cells (ECs) during blood vessel formation. However, the underlying cellular events controlled by different GTPases remain unclear. Here, we assess the cellular mechanisms by which Cdc42 regulates mammalian vascular morphogenesis and maintenance. In vivo deletion of Cdc42 in embryonic ECs (Cdc42(Tie2KO)) results in blocked lumen formation and endothelial tearing, leading to lethality of mutant embryos by E9-10 due to failed blood circulation. Similarly, inducible deletion of Cdc42 (Cdc42(Cad5KO)) at mid-gestation blocks angiogenic tubulogenesis. By contrast, deletion of Cdc42 in postnatal retinal vessels leads to aberrant vascular remodeling and sprouting, as well as markedly reduced filopodia formation. We find that Cdc42 is essential for organization of EC adhesion, as its loss results in disorganized cell-cell junctions and reduced focal adhesions. Endothelial polarity is also rapidly lost upon Cdc42 deletion, as seen by failed localization of apical podocalyxin (PODXL) and basal actin. We link observed failures to a defect in F-actin organization, both in vitro and in vivo, which secondarily impairs EC adhesion and polarity. We also identify Cdc42 effectors Pak2/4 and N-WASP, as well as the actomyosin machinery, to be crucial for EC actin organization. This work supports the notion of Cdc42 as a central regulator of the cellular machinery in ECs that drives blood vessel formation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.