ArticleThe Journal of biological chemistry2012
Myosin regulatory light chain diphosphorylation slows relaxation of arterial smooth muscle.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Smooth muscle contractile cytoskeleton in health and disease.Journal of muscle research and cell motility · 2026Review
- MLC2: Physiological Functions and Potential Roles in Tumorigenesis.Cell biochemistry and biophysics · 2025Review
- Role of ZIP kinase in development of myofibroblast differentiation from HPMCs.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Paxillin participates in the sphingosylphosphorylcholine-induced abnormal contraction of vascular smooth muscle by regulating Rho-kinase activation.Cell communication and signaling : CCS · 2024Article
- Differential expression of the enzymes regulating myosin light chain phosphorylation are responsible for the slower relaxation of pulmonary artery than mesenteric artery in rats.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024Article
- T18/S19 diphosphorylation of myosin regulatory light chain impairs pulmonary artery relaxation in monocrotaline-induced pulmonary hypertensive rats.Pflugers Archiv : European journal of physiology · 2023Article
- Thyroxine Induces Acute Relaxation of Rat Skeletal Muscle Arteries via Integrin αvβ3, ERK1/2 and Integrin-Linked Kinase.Frontiers in physiology · 2021Article
- EPAC in Vascular Smooth Muscle Cells.International journal of molecular sciences · 2020Review
- Article
- Opsin 3 and 4 mediate light-induced pulmonary vasorelaxation that is potentiated by G protein-coupled receptor kinase 2 inhibition.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Gene expression profiles and signaling mechanisms in αBMC systems biology · 2017Article
- Signaling pathways induced by serine proteases to increase intestinal epithelial barrier function.PloS one · 2017Article
- Phosphorylation of the regulatory light chain of myosin in striated muscle: methodological perspectives.European biophysics journal : EBJ · 2016Review
- Phosphorylated Myosin Light Chain 2 (p-MLC2) as a Molecular Marker of Antemortem Coronary Artery Spasm.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
- p21-Activated kinase (Pak) regulates airway smooth muscle contraction by regulating paxillin complexes that mediate actin polymerization.The Journal of physiology · 2016Article
- A novel inhibitory effect of oxazol-5-one compounds on ROCKII signaling in human coronary artery vascular smooth muscle cells.Scientific reports · 2016Article
- Highly sensitive myosin phosphorylation analysis in the renal afferent arteriole.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2016Review
- Attenuated platelet aggregation in patients with septic shock is independent from the activity state of myosin light chain phosphorylation or a reduction in Rho kinase-dependent inhibition of myosin light chain phosphatase.Intensive care medicine experimental · 2015Article
- A role for the Ca(2+)-dependent tyrosine kinase Pyk2 in tonic depolarization-induced vascular smooth muscle contraction.Journal of muscle research and cell motility · 2015Review
- A role for the tyrosine kinase Pyk2 in depolarization-induced contraction of vascular smooth muscle.The Journal of biological chemistry · 2015Article
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2 authors.
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Abstract
The principal signal to activate smooth muscle contraction is phosphorylation of the regulatory light chains of myosin (LC(20)) at Ser(19) by Ca(2+)/calmodulin-dependent myosin light chain kinase. Inhibition of myosin light chain phosphatase leads to Ca(2+)-independent phosphorylation at both Ser(19) and Thr(18) by integrin-linked kinase and/or zipper-interacting protein kinase. The functional effects of phosphorylation at Thr(18) on steady-state isometric force and relaxation rate were investigated in Triton-skinned rat caudal arterial smooth muscle strips. Sequential phosphorylation at Ser(19) and Thr(18) was achieved by treatment with adenosine 5'-O-(3-thiotriphosphate) in the presence of Ca(2+), which induced stoichiometric thiophosphorylation at Ser(19), followed by microcystin (phosphatase inhibitor) in the absence of Ca(2+), which induced phosphorylation at Thr(18). Phosphorylation at Thr(18) had no effect on steady-state force induced by Ser(19) thiophosphorylation. However, phosphorylation of Ser(19) or both Ser(19) and Thr(18) to comparable stoichiometries (0.5 mol of P(i)/mol of LC(20)) and similar levels of isometric force revealed differences in the rates of dephosphorylation and relaxation following removal of the stimulus: t(½) values for dephosphorylation were 83.3 and 560 s, and for relaxation were 560 and 1293 s, for monophosphorylated (Ser(19)) and diphosphorylated LC(20), respectively. We conclude that phosphorylation at Thr(18) decreases the rates of LC(20) dephosphorylation and smooth muscle relaxation compared with LC(20) phosphorylated exclusively at Ser(19). These effects of LC(20) diphosphorylation, combined with increased Ser(19) phosphorylation (Ca(2+)-independent), may underlie the hypercontractility that is observed in response to certain physiological contractile stimuli, and under pathological conditions such as cerebral and coronary arterial vasospasm, intimal hyperplasia, and hypertension.
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