ArticleAmerican journal of physiology. Cell physiology2010
TRPC-mediated actin-myosin contraction is critical for BBB disruption following hypoxic stress.
Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 70 citations in OpenAlex.
- Article
- Muscone Reduces OGD/R-Induced Hyperpermeability of the Brain Endothelial Barrier by Activating the PKA/RHOA/MLC Pathway.Current neurovascular research · 2025Article
- Tension at the gate: sensing mechanical forces at the blood-brain barrier in health and disease.Journal of neuroinflammation · 2024Review
- Trifluoperazine regulates blood-brain barrier permeability via the MLCK/p-MLC pathway to promote ischemic stroke recovery.iScience · 2024Article
- Kv7 channel activation reduces brain endothelial cell permeability and prevents kainic acid-induced blood-brain barrier damage.American journal of physiology. Cell physiology · 2024Article
- Inhibition of UTX/KDM6A improves recovery of spinal cord injury by attenuating BSCB permeability and macrophage infiltration through the MLCK/p-MLC pathway.Journal of neuroinflammation · 2023Article
- Mechanisms of Blood-Brain Barrier Protection by Microbiota-Derived Short-Chain Fatty Acids.Cells · 2023Review
- Ion Channels in Gliomas-From Molecular Basis to Treatment.International journal of molecular sciences · 2023Review
- Blood-brain barrier leakage in Alzheimer's disease: From discovery to clinical relevance.Pharmacology & therapeutics · 2022Review
- Hypoxia-induced blood-brain barrier dysfunction is prevented by pericyte-conditioned media via attenuated actomyosin contractility and claudin-5 stabilization.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Blood-Brain Barrier Dysfunction in CNS Disorders and Putative Therapeutic Targets: An Overview.Pharmaceutics · 2021Review
- Gastrointestinal motility modulation by stress is associated with reduced smooth muscle contraction through specific transient receptor potential channel.The Journal of veterinary medical science · 2021Article
- Yuzu and Hesperidin Ameliorate Blood-Brain Barrier Disruption during Hypoxia via Antioxidant Activity.Antioxidants (Basel, Switzerland) · 2020Article
- Modeling blood-brain barrier pathology in cerebrovascular disease in vitro: current and future paradigms.Fluids and barriers of the CNS · 2020Review
- TRP Channels and Small GTPases Interplay in the Main Hallmarks of Metastatic Cancer.Frontiers in pharmacology · 2020Review
- CaAdvances in cancer research · 2020Review
- Article
- Blood-Brain Barrier: From Physiology to Disease and Back.Physiological reviews · 2019Review
- A TR(i)P to Cell Migration: New Roles of TRP Channels in Mechanotransduction and Cancer.Frontiers in physiology · 2019Review
- Kv1.3 activity perturbs the homeostatic properties of astrocytes in glioma.Scientific reports · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Hypoxia-induced disruption of the blood-brain barrier (BBB) is the result of many different mechanisms, including alterations to the cytoskeleton. In this study, we identified actin-binding proteins involved in cytoskeletal dynamics with quantitative proteomics and assessed changes in subcellular localization of two proteins involved in actin polymerization [vasodilator-stimulated phosphoprotein (VASP)] and cytoskeleton-plasma membrane cross-linking (moesin). We found significant redistribution of both VASP and moesin to the cytoskeletal and membrane fractions of BBB endothelial cells after 1-h hypoxic stress. We also investigated activation of actin-myosin contraction through assessment of phosphorylated myosin light chain (pMLC) with confocal microscopy. Hypoxia caused a rapid and transient increase in pMLC. Blocking MLC phosphorylation through inhibition of myosin light chain kinase (MLCK) with ML-7 prevented hypoxia-induced BBB disruption and relocalization of the tight junction protein ZO-1. Finally, we implicate the transient receptor potential (TRP)C family of channels in mediating these events since blockade of TRPC channels and the associated calcium influx with SKF-96365 prevents hypoxia-induced permeability changes and the phosphorylation of MLC needed for actin-myosin contraction. These data suggest that hypoxic stress triggers alterations to cytoskeletal structure that contribute to BBB disruption and that calcium influx through TRPC channels contributes to these events.
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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.