ArticleThe Journal of physiology2003
Essential role of rho kinase in the Ca2+ sensitization of prostaglandin F(2alpha)-induced contraction of rabbit aortae.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 84 citations in OpenAlex.
- Articular Chondrocyte Phenotype Regulation through the Cytoskeleton and the Signaling Processes That Originate from or Converge on the Cytoskeleton: Towards a Novel Understanding of the Intersection between Actin Dynamics and Chondrogenic Function.International journal of molecular sciences · 2021Review
- Ryanodine-induced vasoconstriction of the gerbil spiral modiolar artery depends on the CaBMC physiology · 2016Article
- MYPT1 isoforms expressed in HEK293T cells are differentially phosphorylated after GTPγS treatment.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2016Article
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- Phasic contractions of isolated human myometrium are associated with Rho-kinase (ROCK)-dependent phosphorylation of myosin phosphatase-targeting subunit (MYPT1).Molecular human reproduction · 2012Article
- Enhancement of myofilament calcium sensitivity by acute hypoxia in rat distal pulmonary arteries.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- A novel biased allosteric compound inhibitor of parturition selectively impedes the prostaglandin F2alpha-mediated Rho/ROCK signaling pathway.The Journal of biological chemistry · 2010Article
- Correspondence between neurological deficit, cerebral infarct size, and Rho-kinase activity in a rat cerebral thrombosis model.Journal of molecular neuroscience : MN · 2009Article
- Myosin light chain kinase activation and calcium sensitization in smooth muscle in vivo.American journal of physiology. Cell physiology · 2008Article
- Interaction between src family kinases and rho-kinase in agonist-induced Ca2+-sensitization of rat pulmonary artery.Cardiovascular research · 2008Article
- PKC and Rho in vascular smooth muscle: activation by BOXes and SAH CSF.Frontiers in bioscience : a journal and virtual library · 2008Article
- Rho kinase (ROCK) inhibitors.Journal of cardiovascular pharmacology · 2007Review
- Rho-kinase-mediated regulation of receptor-agonist-stimulated smooth muscle contraction.Pflugers Archiv : European journal of physiology · 2006Article
- Mechanisms of the prostaglandin F2alpha-induced rise in [Ca2+]i in rat intrapulmonary arteries.The Journal of physiology · 2006Article
- Interaction between spontaneous and neurally mediated regulation of smooth muscle tone in the rabbit corpus cavernosum.The Journal of physiology · 2005Article
- Integrin-linked kinase is responsible for Ca2+-independent myosin diphosphorylation and contraction of vascular smooth muscle.The Biochemical journal · 2005Article
- Thromboxane A2-induced contraction of rat caudal arterial smooth muscle involves activation of Ca2+ entry and Ca2+ sensitization: Rho-associated kinase-mediated phosphorylation of MYPT1 at Thr-855, but not Thr-697.The Biochemical journal · 2005Article
- Role of contractile prostaglandins and Rho-kinase in growth factor-induced airway smooth muscle contraction.Respiratory research · 2005Article
- Inhibition of protein kinase C-mediated contraction by Rho kinase inhibitor fasudil in rabbit aorta.Naunyn-Schmiedeberg's archives of pharmacology · 2004Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inhibition of dephosphorylation of the 20 kDa myosin light chain (MLC(20)) is an important mechanism for the Ca(2+)-induced sensitization of vascular smooth muscle contraction. We investigated whether this mechanism operates in prostaglandin F(2alpha) (PGF(2alpha))-induced contraction of rabbit aortic smooth muscle and, if so, whether protein kinase C (PKC) or rho-associated kinase (rho kinase) contribute to the inhibition of dephosphorylation. In normal medium, PGF(2alpha) (10 microM) increased the phosphorylation of MLC(20) and developed tension. The rho-kinase inhibitors fasudil and hydroxyfasudil inhibited these changes, despite having no effect on a phorbol-ester-induced MLC(20) phosphorylation. After treatment with verapamil or chelation of external Ca(2+) with EGTA, PGF(2alpha) increased the MLC(20) phosphorylation and tension without an increase in [Ca(2+)](i), all of which were sensitive to fasudil and hydroxyfasudil. ML-9, a MLC kinase inhibitor, quickly reversed the KCl-induced MLC(20) phosphorylation and contraction to the resting level. However, fractions of PGF(2alpha)-induced contraction and MLC(20) phosphorylation were resistant to ML-9 but were sensitive to fasudil. Ro31-8220 (10 microM), a PKC inhibitor, did not affect the phosphorylation of MLC(20) and the tension caused by PGF(2alpha), thus excluding the possibility of the involvement of PKC in the PGF(2alpha)-induced MLC(20) phosphorylation. PGF(2alpha) increased phosphorylation at Thr654 of the myosin binding subunit (MBS) of myosin phosphatase, which is a target of rho kinase, and fasudil decreased the phosphorylation. These data suggest that the PGF(2alpha)-induced contraction is accompanied by the inhibition of MLC(20) dephosphorylation through rho kinase-induced MBS phosphorylation, leading to Ca(2+) sensitization of contraction. An actin-associated mechanism may also be involved in the PGF(2alpha)-induced sensitization.
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