Document Detail


Inhibition of Rho-kinase leads to rapid activation of phosphatidylinositol 3-kinase/protein kinase Akt and cardiovascular protection.
MedLine Citation:
PMID:  15319269     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Rho-kinase activity is increased in cardiovascular diseases and in patients with cardiovascular risk factors. However, it is not known whether inhibition of Rho-kinase could lead to cardiovascular protection and, if so, by what mechanism.
METHODS AND RESULTS: In human endothelial cells, the Rho-kinase inhibitor, hydroxyfasudil (HF) (1 to 100 micromol/L), increased Akt serine-473 phosphorylation within 15 minutes, leading to a 2.2-fold and 4.0-fold increase in Akt kinase activity and nitric oxide (NO) release, respectively. Activation of Akt and eNOS by HF was completely blocked by the phosphatidylinositol 3-kinase (PI3-kinase) inhibitor, LY294002 (10 micromol/L). To determine the physiological relevance of this pathway, we used 2 models of ischemia-reperfusion (I/R) injury. Acute administration of fasudil (10 mg/kg, intraperitoneal, 1 hour before ischemia) decreased leukocyte recruitment and adhesion to the mesenteric endothelium after I/R injury in wild-type but not eNOS-/- mice. Similarly, treatment with fasudil decreased myocardial infarct size by 38% in rats subjected to transient coronary artery occlusion. Cotreatment with 2 PI3-kinase inhibitors, wortmannin and LY294002, or the eNOS inhibitor, L-NAME, blocked the cardiovascular protective effects of fasudil.
CONCLUSIONS: Inhibition of Rho-kinase leads to the activation of the PI3-kinase/Akt/eNOS pathway and cardiovascular protection. These findings suggest that Rho-kinase may play an important role in mediating the inflammatory response to I/R injury.
Authors:
Sebastian Wolfrum; Andreas Dendorfer; Yoshiyuki Rikitake; Timothy J Stalker; Yulan Gong; Rosario Scalia; Peter Dominiak; James K Liao
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2004-08-19
Journal Detail:
Title:  Arteriosclerosis, thrombosis, and vascular biology     Volume:  24     ISSN:  1524-4636     ISO Abbreviation:  Arterioscler. Thromb. Vasc. Biol.     Publication Date:  2004 Oct 
Date Detail:
Created Date:  2004-10-08     Completed Date:  2005-03-24     Revised Date:  2012-06-22    
Medline Journal Info:
Nlm Unique ID:  9505803     Medline TA:  Arterioscler Thromb Vasc Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1842-7     Citation Subset:  IM    
Affiliation:
Vascular Medicine Research Unit, Brigham & Women's Hospital and Harvard Medical School, Cambridge, Mass 02139, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cardiovascular System / enzymology*
Enzyme Activation / physiology
Heart Diseases / prevention & control
Humans
Intracellular Signaling Peptides and Proteins
Male
Mice
Mice, Inbred C57BL
Nitric Oxide Synthase / metabolism
Nitric Oxide Synthase Type II
Nitric Oxide Synthase Type III
Phosphatidylinositol 3-Kinases / metabolism*
Protein-Serine-Threonine Kinases / antagonists & inhibitors*,  metabolism*
Proto-Oncogene Proteins / metabolism*
Proto-Oncogene Proteins c-akt
Rats
Rats, Wistar
Vascular Diseases / prevention & control
rho-Associated Kinases
Grant Support
ID/Acronym/Agency:
DK-64344/DK/NIDDK NIH HHS; HL-52233/HL/NHLBI NIH HHS; P01 HL048743-120008/HL/NHLBI NIH HHS; P01 NS010828-330036/NS/NINDS NIH HHS; R01 DK062729-01A1/DK/NIDDK NIH HHS; R01 HL052233-05/HL/NHLBI NIH HHS; R01 HL052233-06/HL/NHLBI NIH HHS; R01 HL052233-07/HL/NHLBI NIH HHS; R01 HL070274-01/HL/NHLBI NIH HHS; R01 HL070274-02/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Intracellular Signaling Peptides and Proteins; 0/Proto-Oncogene Proteins; EC 1.14.13.39/NOS3 protein, human; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type II; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.14.13.39/Nos3 protein, mouse; EC 1.14.13.39/Nos3 protein, rat; EC 2.7.1.-/Phosphatidylinositol 3-Kinases; EC 2.7.11.1/AKT1 protein, human; EC 2.7.11.1/Akt1 protein, rat; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.1/rho-Associated Kinases
Comments/Corrections
Comment In:
Arterioscler Thromb Vasc Biol. 2005 Apr;25(4):e34; author reply e34-5   [PMID:  15790936 ]

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