ArticleThe Biochemical journal2006
Class II phosphoinositide 3-kinase alpha-isoform regulates Rho, myosin phosphatase and contraction in vascular smooth muscle.
Article in The Biochemical journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 88 citations in OpenAlex.
- Effective treatment of hypertension by recombinant Lactobacillus plantarum expressing angiotensin converting enzyme inhibitory peptide.Microbial cell factories · 2015Trial
- Novel role of the class II α-isoform of phosphatidylinositol 3-kinase in hepatocellular carcinoma: suppressing metastasis by targeting Wnt/β-catenin signaling via inhibiting phosphorylation of LRP6.Cancer cell international · 2026Article
- Inositol metabolism as a broad-spectrum antiviral target.Frontiers in microbiology · 2025Review
- A Novel Single-Color FRET Sensor for Rho-Kinase Reveals Calcium-Dependent Activation of RhoA and ROCK.Sensors (Basel, Switzerland) · 2024Article
- Follicle stimulating hormone promotes production of renin through its receptor in juxtaglomerular cells of kidney.Diabetology & metabolic syndrome · 2022Article
- PI3K Isoforms in Vascular Biology, A Focus on the Vascular System-Immune Response Connection.Current topics in microbiology and immunology · 2022Article
- An Overview of Class II Phosphoinositide 3-Kinases.Current topics in microbiology and immunology · 2022Article
- Class II phosphatidylinositol 3-kinase isoforms in vesicular trafficking.Biochemical Society transactions · 2021Review
- Class II phosphatidylinositol 3-kinase α and β isoforms are required for vascular smooth muscle Rho activation, contraction and blood pressure regulation in mice.The journal of physiological sciences : JPS · 2020Article
- Class II PI3Ks at the Intersection between Signal Transduction and Membrane Trafficking.Biomolecules · 2019Review
- Role of Phosphatidylinositol 3-Kinase (PI3K), Mitogen-Activated Protein Kinase (MAPK), and Protein Kinase C (PKC) in Calcium Signaling Pathways Linked to the αFrontiers in physiology · 2019Article
- PI3K class II α regulates δ-opioid receptor export from theMolecular biology of the cell · 2017Article
- Inhibition of PI3K promotes dilation of human small airways in a rho kinase-dependent manner.British journal of pharmacology · 2016Article
- Sevoflurane and isoflurane inhibit KCl-induced Class II phosphoinositide 3-kinase α subunit mediated vasoconstriction in rat aorta.BMC anesthesiology · 2016Article
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- Insulin augments serotonin-induced contraction via activation of the IR/PI3K/PDK1 pathway in the rat carotid artery.Pflugers Archiv : European journal of physiology · 2016Article
- 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
- Phosphatidylinositol 3-kinase class II α-isoform PI3K-C2α is required for transforming growth factor β-induced Smad signaling in endothelial cells.The Journal of biological chemistry · 2015Article
- Essential role of class II phosphatidylinositol-3-kinase-C2α in sphingosine 1-phosphate receptor-1-mediated signaling and migration in endothelial cells.The Journal of biological chemistry · 2013Article
- Membrane depolarization-induced RhoA/Rho-associated kinase activation and sustained contraction of rat caudal arterial smooth muscle involves genistein-sensitive tyrosine phosphorylation.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2013Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We demonstrated previously that membrane depolarization and excitatory receptor agonists such as noradrenaline induce Ca2+-dependent Rho activation in VSM (vascular smooth muscle), resulting in MP (myosin phosphatase) inhibition through the mechanisms involving Rho kinase-mediated phosphorylation of its regulatory subunit MYPT1. In the present study, we show in de-endothelialized VSM strips that the PI3K (phosphoinositide 3-kinase) inhibitors LY294002 and wortmannin inhibited KCl membrane depolarization- and noradrenaline-induced Rho activation and MYPT1 phosphorylation, with concomitant inhibition of MLC (20-kDa myosin light chain) phosphorylation and contraction. LY294002 also augmented de-phosphorylation of MLC and resultantly relaxation in KCl-contracted VSM, whereas LY294002 was much less effective or ineffective under the conditions in which MP was inhibited by either a phosphatase inhibitor or a phorbol ester in Rho-independent manners. VSM express at least four PI3K isoforms, including the class I enzymes p110alpha and p110beta and the class II enzymes PI3K-C2alpha and -C2beta. The dose-response relationships of PI3K-inhibitor-induced inhibition of Rho, MLC phosphorylation and contraction were similar to that of PI3K-C2alpha inhibition, but not to that of the class I PI3K inhibition. Moreover, KCl and noradrenaline induced stimulation of PI3K-C2alpha in a Ca2+-dependent manner, but not of p110alpha or p110beta. Down-regulation of PI3K-C2alpha expression by siRNA (small interfering RNA) inhibited contraction and phosphorylation of MYPT1 and MLC in VSM cells. Finally, intravenous wortmannin infusion induced sustained hypotension in rats, with inhibition of PI3K-C2alpha activity, GTP-loading of Rho and MYPT1 phosphorylation in the artery. These results indicate the novel role of PI3K-C2alpha in Ca2+-dependent Rho-mediated negative control of MP and thus VSM contraction.
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