ArticleArteriosclerosis, thrombosis, and vascular biology2003
Grb2 is required for the development of neointima in response to vascular injury.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Proteomic Analysis of Prehypertensive and Hypertensive Patients: Exploring the Role of the Actin Cytoskeleton.International journal of molecular sciences · 2024Article
- Bioinformatic Analysis of Coronary Disease Associated SNPs and Genes to Identify Proteins Potentially Involved in the Pathogenesis of Atherosclerosis.Journal of proteomics and genomics research · 2017Article
- Deletion of Methionine Sulfoxide Reductase A Does Not Affect Atherothrombosis but Promotes Neointimal Hyperplasia and Extracellular Signal-Regulated Kinase 1/2 Signaling.Arteriosclerosis, thrombosis, and vascular biology · 2015Article
- Identification of target antigens of anti-endothelial cell and anti-vascular smooth muscle cell antibodies in patients with giant cell arteritis: a proteomic approach.Arthritis research & therapy · 2011Article
- MAPK signalling in cardiovascular health and disease: molecular mechanisms and therapeutic targets.Clinical science (London, England : 1979) · 2008Review
- Requirement for p38 mitogen-activated protein kinase activity in neointima formation after vascular injury.Circulation · 2008Article
- Nf1+/- mice have increased neointima formation via hyperactivation of a Gleevec sensitive molecular pathway.Human molecular genetics · 2008Article
- GRB2-mediated recruitment of GAB2, but not GAB1, to SF-STK supports the expansion of Friend virus-infected erythroid progenitor cells.Oncogene · 2006Article
- Regulation of vascular smooth muscle cell growth: targeting the final common pathway.Arteriosclerosis, thrombosis, and vascular biology · 2003Article
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6 authors.
Funding
Abstract
objectiveNeointima formation occurs in arteries in response to mechanical or chemical injury and is responsible for substantial morbidity. In this work, the role of the intracellular linker protein Grb2 in the pathogenesis of neointima formation was examined. Grb2 is a critical signaling protein that facilitates the activation of the small GTPase ras by receptor tyrosine kinases. METHODS AND
resultsCultured rat aortic smooth muscle cells were treated with an antisense morpholino to Grb2 and these cells showed a reduced proliferative response to platelet-derived growth factor stimulation. Grb2-/- mice do not survive embryonic development. Grb2+/- mice appear normal at birth and are fertile but have defective signaling in several tissues. Cultured smooth muscle cells derived from Grb2+/- mice grew at a much slower rate than cells derived from Grb2+/+ mice. Grb2+/- and Grb2+/+ mice were subjected to carotid injury. After 21 days, Grb2+/+ mice developed robust neointima formation that, in some cases, resulted in an occlusive lesion. In contrast, Grb2+/- mice were resistant to the development of neointima
conclusionsGrb2 is an essential component of the signaling cascade resulting in neointima formation after arterial injury.
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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.