ArticleMolecular and cellular biology2014
Genetic dissection of the vav2-rac1 signaling axis in vascular smooth muscle cells.
Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- VAV2 orchestrates the interplay between regenerative proliferation and ribogenesis in both keratinocytes and oral squamous cell carcinoma.Scientific reports · 2024Article
- Vav2 promotes ductus arteriosus anatomic closure via the remodeling of smooth muscle cells by Rac1 activation.Journal of molecular medicine (Berlin, Germany) · 2023Article
- The Rho GTPase exchange factor Vav2 promotes extensive age-dependent rewiring of the hair follicle stem cell transcriptome.Frontiers in cell and developmental biology · 2023Article
- The Rho guanosine nucleotide exchange factors Vav2 and Vav3 modulate epidermal stem cell function.Oncogene · 2022Article
- Review
- New Functions of Vav Family Proteins in Cardiovascular Biology, Skeletal Muscle, and the Nervous System.Biology · 2021Review
- Repositioning metformin and propranolol for colorectal and triple negative breast cancers treatment.Scientific reports · 2021Article
- Vav2 catalysis-dependent pathways contribute to skeletal muscle growth and metabolic homeostasis.Nature communications · 2020Article
- VAV2 signaling promotes regenerative proliferation in both cutaneous and head and neck squamous cell carcinoma.Nature communications · 2020Article
- Article
- Vav2 pharmaco-mimetic mice reveal the therapeutic value and caveats of the catalytic inactivation of a Rho exchange factor.Oncogene · 2020Article
- DDR1 (Discoidin Domain Receptor-1)-RhoA (Ras Homolog Family Member A) Axis Senses Matrix Stiffness to Promote Vascular Calcification.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Next Generation Sequencing Identify Rare Copy Number Variants in Non-syndromic Patent Ductus Arteriosus.Frontiers in genetics · 2020Article
- Next-generation sequencing identifies novel genes with rare variants in total anomalous pulmonary venous connection.EBioMedicine · 2018Article
- Sustained Activation of Rho GTPases Promotes a Synthetic Pulmonary Artery Smooth Muscle Cell Phenotype in Neprilysin Null Mice.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- p115 RhoGEF activates the Rac1 GTPase signaling cascade in MCP1 chemokine-induced vascular smooth muscle cell migration and proliferation.The Journal of biological chemistry · 2017Article
- Metformin and propranolol combination prevents cancer progression and metastasis in different breast cancer models.Oncotarget · 2017Article
- Article
- MST3 promotes proliferation and tumorigenicity through the VAV2/Rac1 signal axis in breast cancer.Oncotarget · 2016Article
- Vav family exchange factors: an integrated regulatory and functional view.Small GTPases · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular smooth muscle cells (vSMCs) are key in the regulation of blood pressure and the engagement of vascular pathologies, such as hypertension, arterial remodeling, and neointima formation. The role of the Rac1 GTPase in these cells remains poorly characterized. To clarify this issue, we have utilized genetically engineered mice to manipulate the signaling output of Rac1 in these cells at will using inducible, Cre-loxP-mediated DNA recombination techniques. Here, we show that the expression of an active version of the Rac1 activator Vav2 exclusively in vSMCs leads to hypotension as well as the elimination of the hypertension induced by the systemic loss of wild-type Vav2. Conversely, the specific depletion of Rac1 in vSMCs causes defective nitric oxide vasodilation responses and hypertension. Rac1, but not Vav2, also is important for neointima formation but not for hypertension-driven vascular remodeling. These animals also have allowed us to dismiss etiological connections between hypertension and metabolic disease and, most importantly, identify pathophysiological programs that cooperate in the development and consolidation of hypertensive states caused by local vascular tone dysfunctions. Finally, our results suggest that the therapeutic inhibition of Rac1 will be associated with extensive cardiovascular system-related side effects and identify pharmacological avenues to circumvent them.
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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.