ArticleAmerican journal of physiology. Cell physiology2004
Rho-kinase-mediated Ca2+-independent contraction in rat embryo fibroblasts.
Article in American journal of physiology. Cell physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 58 citations in OpenAlex.
- Investigating the Cardiovascular Benefits of Dapagliflozin: Vasodilatory Effect on Isolated Rat Coronary Arteries.International journal of molecular sciences · 2023Article
- Diverse patterns of molecular changes in the mechano-responsiveness of focal adhesions.Scientific reports · 2018Article
- Effects of chemerin/CMKLR1 in obesity-induced hypertension and potential mechanism.American journal of translational research · 2017Article
- Tissue constructs: platforms for basic research and drug discovery.Interface focus · 2016Article
- Kinase-interacting substrate screening is a novel method to identify kinase substrates.The Journal of cell biology · 2015Article
- Protease-activated receptor 1 inhibition by SCH79797 attenuates left ventricular remodeling and profibrotic activities of cardiac fibroblasts.Journal of cardiovascular pharmacology and therapeutics · 2013Article
- Article
- Signaling through myosin light chain kinase in smooth muscles.The Journal of biological chemistry · 2013Article
- MLCK-independent phosphorylation of MLC20 and its regulation by MAP kinase pathway in human bladder smooth muscle cells.Cytoskeleton (Hoboken, N.J.) · 2011Article
- RhoA inactivation prevents photoreceptor axon retraction in an in vitro model of acute retinal detachment.Investigative ophthalmology & visual science · 2011Article
- Real-time monitoring of angiotensin II-induced contractile response and cytoskeleton remodeling in individual cells by atomic force microscopy.Pflugers Archiv : European journal of physiology · 2009Article
- Substrate rigidity regulates Ca2+ oscillation via RhoA pathway in stem cells.Journal of cellular physiology · 2009Article
- Surface Plasmon Resonance Monitoring of Cell Monolayer Integrity: Implication of Signaling Pathways Involved in Actin-Driven Morphological Remodeling.Cellular and molecular bioengineering · 2008Article
- Nonmuscle myosin II is responsible for maintaining endothelial cell basal tone and stress fiber integrity.American journal of physiology. Cell physiology · 2008Article
- A biosensor of S100A4 metastasis factor activation: inhibitor screening and cellular activation dynamics.Biochemistry · 2008Article
- Sustained contraction and loss of NO production in TGFbeta1-treated endothelial cells.British journal of pharmacology · 2006Article
- Signaling mechanism of thrombin-induced gingival fibroblast-populated collagen gel contraction.British journal of pharmacology · 2006Article
- Responses of fibroblasts to anchorage of dorsal extracellular matrix receptors.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
Thus far, determining the relative contribution of Ca2+/calmodulin-dependent myosin light chain kinase (MLCK) and Ca2+-independent Rho-kinase pathways to myosin II activation and contraction has been difficult. In this study, we characterize the role of Rho-kinase in a rat embryo fibroblast cell line (REF-52), which contains no detectable MLCK. No endogenous MLCK could be detected in REF-52 cells by either Western or Northern blot analysis. In the presence or absence of Ca2+, thrombin or lysophosphatidic acid (LPA) increased RhoA activity and Rhokinase activity, correlating with isometric tension development and myosin II regulatory light chain (RLC) phosphorylation. Resting tension is associated with a basal phosphorylation of 0.31 +/- 0.02 mol PO4/mol RLC, whereas upon LPA or thrombin treatment myosin II RLC phosphorylation increases to 1.08 +/- 0.05 and 0.82 +/- 0.05 mol PO4/mol RLC, respectively, within 2.5 min. Ca2+ chelation has minimal effect on the kinetics and magnitude of isometric tension development and RLC phosphorylation. Treatment of REF-52 cells with the Rho-kinase-specific inhibitor Y-27632 abolished thrombin- and LPA-stimulated contraction and RLC phosphorylation. These results suggest that Rho-kinase is sufficient to activate myosin II motor activity and contraction in REF-52 cells.
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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.