ArticleAmerican journal of physiology. Cell physiology2013
Vasoconstrictor-induced endocytic recycling regulates focal adhesion protein localization and function in vascular smooth muscle.
Article in American journal of physiology. Cell physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- Dystrophin and dystrophin association protein expression decreases with age in vascular smooth muscle.GeroScience · 2026Article
- Review
- Non-muscle myosin II regulates aortic stiffness through effects on specific focal adhesion proteins and the non-muscle cortical cytoskeleton.Journal of cellular and molecular medicine · 2021Article
- Aortic Stiffness Hysteresis in Isolated Mouse Aortic Segments Is Intensified by Contractile Stimuli, Attenuated by Age, and Reversed by Elastin Degradation.Frontiers in physiology · 2021Article
- Vascular aging, the vascular cytoskeleton and aortic stiffness.Exploration of medicine · 2021Article
- Rescue of tight junctional localization of a claudin-16 mutant D97S by antimalarial medicine primaquine in Madin-Darby canine kidney cells.Scientific reports · 2019Article
- The role of extracellular matrix stiffness in regulating cytoskeletal remodeling via vinculin in synthetic smooth muscle cells.Biochemical and biophysical research communications · 2019Article
- Acute Nitric Oxide Synthase Inhibition Accelerates Transendothelial Insulin Efflux In Vivo.Diabetes · 2018Article
- Reversal of Aging-Induced Increases in Aortic Stiffness by Targeting Cytoskeletal Protein-Protein Interfaces.Journal of the American Heart Association · 2018Article
- MicroRNA-203 mimics age-related aortic smooth muscle dysfunction of cytoskeletal pathways.Journal of cellular and molecular medicine · 2017Article
- Mechanisms of Vascular Smooth Muscle Contraction and the Basis for Pharmacologic Treatment of Smooth Muscle Disorders.Pharmacological reviews · 2016Review
- Cortical actin regulation modulates vascular contractility and compliance in veins.The Journal of physiology · 2015Article
- Non-receptor tyrosine kinases and the actin cytoskeleton in contractile vascular smooth muscle.The Journal of physiology · 2015Review
- Vascular smooth muscle cell stiffness and adhesion to collagen I modified by vasoactive agonists.PloS one · 2015Article
- Aging impairs smooth muscle-mediated regulation of aortic stiffness: a defect in shock absorption function?American journal of physiology. Heart and circulatory physiology · 2014Article
- The contribution of vascular smooth muscle to aortic stiffness across length scales.Microcirculation (New York, N.Y. : 1994) · 2014Review
- Vasoactive agonists exert dynamic and coordinated effects on vascular smooth muscle cell elasticity, cytoskeletal remodelling and adhesion.The Journal of physiology · 2014Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Turnover of focal adhesions (FAs) is known to be critical for cell migration and adhesion of proliferative vascular smooth muscle (VSM) cells. However, it is often assumed that FAs in nonmigratory, differentiated VSM (dVSM) cells embedded in the wall of healthy blood vessels are stable structures. Recent work has demonstrated agonist-induced actin polymerization and Src-dependent FA phosphorylation in dVSM cells, suggesting that agonist-induced FA remodeling occurs. However, the mechanisms and extent of FA remodeling are largely unknown in dVSM. Here we show, for the first time, that a distinct subpopulation of dVSM FA proteins, but not the entire FA, remodels in response to the α-agonist phenylephrine. Vasodilator-stimulated phosphoprotein and zyxin displayed the largest redistributions, while β-integrin and FA kinase showed undetectable redistribution. Vinculin, metavinculin, Src, Crk-associated substrate, and paxillin displayed intermediate degrees of redistribution. Redistributions into membrane fractions were especially prominent, suggesting endosomal mechanisms. Deconvolution microscopy, quantitative colocalization analysis, and Duolink proximity ligation assays revealed that phenylephrine increases the association of FA proteins with early endosomal markers Rab5 and early endosomal antigen 1. Endosomal disruption with the small-molecule inhibitor primaquine inhibits agonist-induced redistribution of FA proteins, confirming endosomal recycling. FA recycling was also inhibited by cytochalasin D, latrunculin B, and colchicine, indicating that the redistribution is actin- and microtubule-dependent. Furthermore, inhibition of endosomal recycling causes a significant inhibition of the rate of development of agonist-induced dVSM contractions. Thus these studies are consistent with the concept that FAs in dVSM cells, embedded in the wall of the aorta, remodel during the action of a vasoconstrictor.
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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.