ArticleThe Journal of physiology2009
Ca2+ sensitization via phosphorylation of myosin phosphatase targeting subunit at threonine-855 by Rho kinase contributes to the arterial myogenic response.
Article in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 114 citations in OpenAlex.
- Advances in Understanding Calcium Sensitization in Gastrointestinal Smooth Muscles: Pathways, Interstitial Cells, and Disease.Journal of neurogastroenterology and motility · 2026Review
- Differential effect of pulsatile pressure on the myogenic responses of small arteries.Pflugers Archiv : European journal of physiology · 2025Article
- A computational framework for quantifying blood flow dynamics across myogenically-active cerebral arterial networks.Biomechanics and modeling in mechanobiology · 2025Article
- Functional bias of contractile control in mouse resistance arteries.Scientific reports · 2024Article
- Milestone Papers on Signal Transduction Mechanisms of Hypertension and Its Complications.Hypertension (Dallas, Tex. : 1979) · 2024Review
- Effect of Kaempferol on Modulation of Vascular Contractility Mainly through PKC and CPI-17 Inactivation.Biomolecules & therapeutics · 2024Article
- A new model for evaluating pressure-induced vascular tone in small cerebral arteries.Biomechanics and modeling in mechanobiology · 2024Article
- The vascular Na,K-ATPase: clinical implications in stroke, migraine, and hypertension.Clinical science (London, England : 1979) · 2023Review
- Death-associated protein kinase 3 regulates the myogenic reactivity of cerebral arteries.Experimental physiology · 2023Article
- Chemo-mechanical modeling of smooth muscle cell activation for the simulation of arterial walls under changing blood pressure.Biomechanics and modeling in mechanobiology · 2023Article
- Vascular mechanotransduction.Physiological reviews · 2023Review
- The Effect of Luteolin on the Modulation of Vascular Contractility via ROCK and CPI-17 Inactivation.Biomolecules & therapeutics · 2023Article
- Myosin light chain phosphorylation exhibits a gradient across the wall of cerebellar arteries under sustained ex vivo vascular tone.Scientific reports · 2023Article
- Effect of Carotid Body Denervation on Systemic Endothelial Function in a Diabetic Animal Model.Advances in experimental medicine and biology · 2023Article
- p90RSK2, a new MLCK mediates contractility in myosin light chain kinase null smooth muscle.Frontiers in physiology · 2023Article
- The Effect of Galangin on the Regulation of Vascular Contractility via the Holoenzyme Reactivation Suppressing ROCK/CPI-17 rather than PKC/CPI-17.Biomolecules & therapeutics · 2022Article
- Regulation of myosin light-chain phosphorylation and its roles in cardiovascular physiology and pathophysiology.Hypertension research : official journal of the Japanese Society of Hypertension · 2022Review
- Cadmium-induced hypertension is associated with renal myosin light chain phosphatase inhibition via increased T697 phosphorylation and p44 mitogen-activated protein kinase levels.Hypertension research : official journal of the Japanese Society of Hypertension · 2021Article
- Characterization of Contractile Machinery of Vascular Smooth Muscles in Hypertension.Life (Basel, Switzerland) · 2021Review
- Cerebral Autoregulation in Subarachnoid Hemorrhage.Frontiers in neurology · 2021Review
12 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Ca(2+) sensitization has been postulated to contribute to the myogenic contraction of resistance arteries evoked by elevation of transmural pressure. However, the biochemical evidence of pressure-induced increases in phosphorylated myosin light chain phosphatase (MLCP) targeting subunit 1 (MYPT1) and/or 17 kDa protein kinase C (PKC)-potentiated protein phosphatase 1 inhibitor protein (CPI-17) required to sustain this view is not currently available. Here, we determined whether Ca(2+) sensitization pathways involving Rho kinase (ROK)- and PKC-dependent phosphorylation of MYPT1 and CPI-17, respectively, contribute to the myogenic response of rat middle cerebral arteries. ROK inhibitors (Y27632, 0.03-10 micromol l(-1); H1152, 0.001-0.3 micromol l(-1)) and PKC inhibitors (GF109203X, 3 micromol l(-1); Gö6976; 10 micromol l(-1)) suppressed myogenic vasoconstriction between 40 and 120 mmHg. An improved, highly sensitive 3-step Western blot method was developed for detection and quantification of MYPT1 and CPI-17 phosphorylation. Increasing pressure from 10 to 60 or 100 mmHg significantly increased phosphorylation of MYPT1 at threonine-855 (T855) and myosin light chain (LC(20)). Phosphorylation of MYPT1 at threonine-697 (T697) and CPI-17 were not affected by pressure. Pressure-evoked elevations in MYPT1-T855 and LC(20) phosphorylation were reduced by H1152, but MYPT1-T697 phosphorylation was unaffected. Inhibition of PKC with GF109203X did not affect MYPT1 or LC(20) phosphorylation at 100 mmHg. Our findings provide the first direct, biochemical evidence that a Ca(2+) sensitization pathway involving ROK-dependent phosphorylation of MYPT1 at T855 (but not T697) and subsequent augmentation of LC(20) phosphorylation contributes to myogenic control of arterial diameter in the cerebral vasculature. In contrast, suppression of the myogenic response by PKC inhibitors cannot be attributed to block of Ca(2+) sensitization mediated by CPI-17 or MYPT1 phosphorylation.
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