scholarly journals Rho‐kinase inhibition by fasudil modulates pre‐synaptic vesicle dynamics

2021 ◽  
Author(s):  
Kim Ann Saal ◽  
Carmina Warth Pérez Arias ◽  
Anna‐Elisa Roser ◽  
Jan Christoph Koch ◽  
Mathias Bähr ◽  
...  
Keyword(s):  
Synaptic Vesicle ◽  
Rho Kinase ◽  
Kinase Inhibition ◽  
Vesicle Dynamics

scholarly journals The Neuroprotective Potential of Rho-Kinase Inhibition in Promoting Cell Survival and Reducing Reactive Gliosis in Response to Hypoxia in Isolated Bovine Retina

2013 ◽  
Vol 32 (1) ◽  
pp. 218-234 ◽  
Author(s):  
Aizhan Alt ◽  
Ralf-Dieter Hilgers ◽  
Aysegül Tura ◽  
Khaled Nassar ◽  
Toni Schneider ◽  
...  
Keyword(s):  
Cell Survival ◽  
Rho Kinase ◽  
Reactive Gliosis ◽  
Kinase Inhibition ◽  
Bovine Retina

scholarly journals Rho-Kinase Inhibition During Early Cardiac Development Causes Arrhythmogenic Right Ventricular Cardiomyopathy in Mice

2015 ◽  
Vol 35 (10) ◽  
pp. 2172-2184 ◽  
Author(s):  
Alia Ellawindy ◽  
Kimio Satoh ◽  
Shinichiro Sunamura ◽  
Nobuhiro Kikuchi ◽  
Kota Suzuki ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Cardiac Development ◽  
Arrhythmogenic Right Ventricular Cardiomyopathy ◽  
Rho Kinase ◽  
Ventricular Cardiomyopathy ◽  
Kinase Inhibition ◽  
Early Cardiac Development

The effect of Rho Kinase inhibition on corneal nerve regeneration in vitro and in vivo

2021 ◽  
Author(s):  
Sonja Mertsch ◽  
Inga Neumann ◽  
Cosima Rose ◽  
Marc Schargus ◽  
Gerd Geerling ◽  
...  
Keyword(s):  
Nerve Regeneration ◽  
Rho Kinase ◽  
Kinase Inhibition ◽  
Corneal Nerve ◽  
Regeneration In Vitro

scholarly journals The atypical structure and function of newborn arterial endothelium is mediated by Rho/Rho kinase signaling

2014 ◽  
Vol 307 (4) ◽  
pp. H628-H632 ◽  
Author(s):  
Sheila Flavahan ◽  
Nicholas A. Flavahan
Keyword(s):  
Laser Scanning ◽  
Rho Kinase ◽  
Laser Scanning Microscopy ◽  
Scanning Microscopy ◽  
Stress Fibers ◽  
Light Chains ◽  
Myosin Light Chains ◽  
Kinase Signaling ◽  
No Donor ◽  
Kinase Inhibition

Endothelium of fetal or newborn arteries is atypical, displaying actin stress fibers and reduced nitric oxide (NO)-mediated dilatation. This study tested the hypothesis that Rho/Rho kinase signaling, which promotes endothelial stress fibers and inhibits endothelial dilatation, contributed to this phenotype. Carotid arteries were isolated from newborn [ postnatal day 1 (P1)], P7, and P21 mice. Endothelial dilatation to acetylcholine (pressure myograph) was minimal at P1, increased at P7, and further increased at P21. Inhibition of Rho (C3 transferase) or Rho kinase (Y27632, fasudil) significantly increased dilatation to acetylcholine in P1 arteries but had no effect in P7 or P21 arteries. After inhibition of NO synthase ( NG-nitro-l-arginine methyl ester), Rho kinase inhibition no longer increased acetylcholine responses in P1 arteries. Rho kinase inhibition did not affect dilatation to the NO donor DEA-NONOate. The endothelial actin cytoskeleton was labeled with phalloidin and visualized by laser-scanning microscopy. In P1 arteries, the endothelium had prominent transcytoplasmic stress fibers, whereas in P7 and P21 arteries, the actin fibers had a significantly reduced intensity and were restricted to cell borders. Phosphorylation of myosin light chains, a Rho kinase substrate, was highest in P1 endothelium and significantly reduced in P7 and P21 endothelium (laser-scanning microscopy). In P1 arteries, inhibition of Rho (C3 transferase) or Rho kinase (Y27632) significantly reduced the intensity of actin fibers, which were restricted to cell borders. Similarly, in P1 arteries, Rho inhibition significantly reduced endothelial levels of phosphorylated myosin light chains. These results indicate that the atypical function and morphology of newborn endothelium is mediated by Rho/Rho kinase signaling.

Induction of the Stem-like Cell Regulator CD44 by Rho Kinase Inhibition Contributes to the Maintenance of Colon Cancer–Initiating Cells

2012 ◽  
Vol 72 (19) ◽  
pp. 5101-5110 ◽  
Author(s):  
Hirokazu Ohata ◽  
Tatsuya Ishiguro ◽  
Yuki Aihara ◽  
Ai Sato ◽  
Hiroaki Sakai ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Rho Kinase ◽  
Kinase Inhibition

scholarly journals EFFECTS OF RHO-KINASE INHIBITION ON ADRENERGIC AND CALCIUM SENSITIVITY IN VASCULAR SMOOTH MUSCLE ASSOCIATED WITH DIABETES MELLITUS: PP.17.135

2010 ◽  
Vol 28 ◽  
pp. e290-e291
Author(s):  
I Kizub ◽  
C Jonson ◽  
O Pavlova ◽  
A Soloviev ◽  
A Zholos
Keyword(s):  
Diabetes Mellitus ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Rho Kinase ◽  
Calcium Sensitivity ◽  
Kinase Inhibition

scholarly journals Rho-Kinase Inhibition Ameliorates Dasatinib-Induced Endothelial Dysfunction and Pulmonary Hypertension

2018 ◽  
Vol 9 ◽  
Author(s):  
Csilla Fazakas ◽  
Chandran Nagaraj ◽  
Diana Zabini ◽  
Attila G. Végh ◽  
Leigh M. Marsh ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Endothelial Dysfunction ◽  
Rho Kinase ◽  
Kinase Inhibition

scholarly journals Rho Kinase Inhibition Is Essential During In Vitro Neurogenesis and Promotes Phenotypic Rescue of Human Induced Pluripotent Stem Cell-Derived Neurons With Oligophrenin-1 Loss of Function

2016 ◽  
Vol 5 (7) ◽  
pp. 860-869 ◽  
Author(s):  
Claudia Compagnucci ◽  
Sabina Barresi ◽  
Stefania Petrini ◽  
Pierre Billuart ◽  
Giorgia Piccini ◽  
...  
Keyword(s):  
Stem Cell ◽  
Pluripotent Stem Cell ◽  
Rho Kinase ◽  
Induced Pluripotent Stem Cell ◽  
Loss Of Function ◽  
Kinase Inhibition ◽  
Induced Pluripotent ◽  
Phenotypic Rescue

Honeycomb Epithelial Edema Associated With Rho Kinase Inhibition

Cornea ◽  
2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Lance J. Lyons ◽  
Kristi Y. Wu ◽  
Keith H. Baratz ◽  
Arthur J. Sit
Keyword(s):  
Rho Kinase ◽  
Kinase Inhibition

Abstract 2474: Rho-Kinase Inhibition Improves Endothelium-Dependent Vasodilation during Hyperinsulinemia in Patients with Metabolic Syndrome

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Francesca Schinzari ◽  
Manfredi Tesauro ◽  
Valentina Rovella ◽  
Augusto Veneziani ◽  
Nadia Mores ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Vascular Function ◽  
Vascular Reactivity ◽  
Rho Kinase ◽  
Serine Phosphorylation ◽  
No Donor ◽  
Kinase Inhibition ◽  
Impaired Insulin

Impaired insulin-mediated vasodilation in the skeletal muscle may be involved in the development of hypertension in patients with metabolic syndrome (MetS) and contribute to insulin resistance by diminishing the glucose uptake. Rho-kinase, an effector of the small G protein Rho A, plays an important role in hypertension and is reported to interfere with insulin signaling through serine phosphorylation of insulin receptor substrate-1 in blood vessels. We therefore examined the role of Rho-kinase in the pathophysiology of impaired vascular reactivity in patients with MetS by evaluating the effect of Rho-kinase inhibition on NO-dependent vasodilation during hyperinsulinemia. Forearm blood flow (FBF) responses to acetylcholine (ACh), a stimulus for endothelial release of NO, and sodium nitroprusside (SNP), an exogenous NO donor, were assessed during insulin administration (0.1 mU/Kg/min) using the forearm perfusion technique in patients with MetS (n=10) and matched controls (n=10). Patients with MetS were then randomized to intra-arterial infusion of either fasudil (inhibitor of Rho-kinase, 200 μg/min) or placebo and reactivity to ACh and SNP was reassessed. During hyperinsulinemia, vasodilator responses to both ACh and SNP were blunted in patients with MetS (both P>0.001 vs. controls). In patients who received fasudil, its administration did not change unstimulated FBF (P=0.75 vs. insulin alone); the vasodilator response to ACh, however, was significantly enhanced by fasudil (P=0.009 vs. insulin alone), while the response to SNP was not significantly changed (P=0.56). In patients with MetS who received placebo, vascular reactivity to both ACh and SNP was not different than before (both P>0.05). In conclusion, Rho-kinase inhibition during hyperinsulinemia improves endothelium-dependent vasodilator responsiveness in patients with MetS. This suggests that, under those conditions, intravascular activation of Rho-kinase is involved in the pathophysiology of endothelial dysfunction and may constitute a critical mediator linking metabolic and hemodynamic abnormalities in insulin resistance. As a consequence, targeting Rho-kinase might beneficially impact both vascular function and insulin sensitivity in patients with MetS.

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