ArticlePloS one2015
Apolipoprotein E3 Inhibits Rho to Regulate the Mechanosensitive Expression of Cox2.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 14 citations in OpenAlex.
- The influences of ApoE isoforms on endothelial adherens junctions and actin cytoskeleton responding to mCRP.Angiogenesis · 2024Article
- Survivin regulates intracellular stiffness and extracellular matrix production in vascular smooth muscle cells.APL bioengineering · 2023Article
- A machine learning pipeline revealing heterogeneous responses to drug perturbations on vascular smooth muscle cell spheroid morphology and formation.Scientific reports · 2021Article
- Stiffness-dependent motility and proliferation uncoupled by deletion of CD44.Scientific reports · 2017Article
- Arterial stiffness induces remodeling phenotypes in pulmonary artery smooth muscle cells via YAP/TAZ-mediated repression of cyclooxygenase-2.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Measuring the Stiffness of Ex Vivo Mouse Aortas Using Atomic Force Microscopy.Journal of visualized experiments : JoVE · 2016Article
- Mechanical heterogeneities in the subendothelial matrix develop with age and decrease with exercise.Journal of biomechanics · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Apolipoprotein E3 (apoE3) is thought to protect against atherosclerosis by enhancing reverse cholesterol transport. However, apoE3 also has cholesterol-independent effects that contribute to its anti-atherogenic properties. These include altering extracellular matrix protein synthesis and inhibiting vascular smooth muscle cell proliferation. Both of these cholesterol-independent effects result from an apoE3-mediated induction of cyclooxygenase-2 (Cox2). Nevertheless, how apoE3 regulates Cox2 remains unknown. Here, we show that apoE3 inhibits the activation of Rho, which reduces the formation of actin stress fibers and focal adhesions and results in cellular softening. Inhibition of Rho-Rho kinase signaling or direct cellular softening recapitulates the effect of apoE3 on Cox2 expression while a constitutively active Rho mutant overrides the apoE3 effect on both intracellular stiffness and Cox2. Thus, our results describe a previously unidentified mechanism by which an atheroprotective apolipoprotein uses Rho to control cellular mechanics and Cox2.
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Registered trials
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