Prevention of diabetes-induced arginase activation and vascular dysfunction by Rho kinase (ROCK) knockout.

@article{Yao2013PreventionOD,
  title={Prevention of diabetes-induced arginase activation and vascular dysfunction by Rho kinase (ROCK) knockout.},
  author={Lin Yao and Surabhi Chandra and Haroldo Af Toque and Anil Bhatta and Modesto Rojas and Ruth B. Caldwell and Robert W. Caldwell},
  journal={Cardiovascular research},
  year={2013},
  volume={97 3},
  pages={
          509-19
        }
}
AIMS We determined the role of the Rho kinase (ROCK) isoforms in diabetes-induced vascular endothelial dysfunction and enhancement of arginase activity and expression. METHODS AND RESULTS Studies were performed in aortic tissues from haplo-insufficient (H-I) ROCK1 and ROCK2 mice and wild-type (WT) mice rendered diabetic with streptozotocin and in bovine aortic endothelial cells (BAECs) treated with high glucose (HG, 25 mM). Protein expression of both ROCK isoforms was substantially elevated… Expand
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References

SHOWING 1-10 OF 47 REFERENCES
Diabetes-induced Coronary Vascular Dysfunction Involves Increased Arginase Activity
TLDR
It is indicated that increased arginase activity in diabetes contributes to vascular endothelial dysfunction by decreasing l-arginine availability to NO synthase. Expand
Diabetes-induced vascular dysfunction involves arginase I.
TLDR
In diabetic WT and AI(+/-)AII (-/-) mice, aortic arginase activity and AI expression were significantly increased compared with control mice, but neither parameter was altered in AI( +/-) aorta, which indicates a major involvement of AI in diabetes-induced vascular dysfunction. Expand
Arginase-2 Mediates Diabetic Renal Injury
TLDR
Findings indicate that arginase-2 plays a major role in induction of diabetic renal injury and that blocking arginases activity or expression could be a novel therapeutic approach for treatment of DN. Expand
Peroxynitrite Mediates Diabetes-Induced Endothelial Dysfunction: Possible Role of Rho Kinase Activation
TLDR
Together, peroxynitrite can suppress eNOS expression via activation of RhoA and hence cause vascular dysfunction, and treatment of diabetic animals with FeTTPS blocked these effects. Expand
Involvement of Rho-kinase in experimental vascular endothelial dysfunction
TLDR
It may be concluded that fasudil prevented DM and HHcy-induced VED partially by decreasing serum glucose and homocysteine concentration due to inhibition of Rho-kinase. Expand
ROCK1 mediates leukocyte recruitment and neointima formation following vascular injury.
TLDR
It is indicated that ROCK1 in BM-derived cells mediates neointima formation following vascular injury and suggest that ROCK 1 may represent a promising therapeutic target in vascular inflammatory diseases. Expand
Inflammatory stimuli upregulate Rho-kinase in human coronary vascular smooth muscle cells.
TLDR
The results indicate that the expression and function of Rho-kinase are upregulated by inflammatory stimuli in hcVSMC with an involvement of PKC and NF-kappaB both in vitro and in vivo. Expand
Arginase inhibition restores NOS coupling and reverses endothelial dysfunction and vascular stiffness in old rats.
TLDR
It is demonstrated that arginase upregulation leads to endothelial nitric oxide synthase (eNOS) uncoupling and that in vivo chronic inhibition of arginases restores nitroso-redox balance, improves endothelial function, and increases vascular compliance in old rats, and suggested that arginsase is a viable target for therapy in age-dependent vascular stiffness. Expand
Involvement of Rho kinase pathway in the mechanism of renal vasoconstriction and cardiac hypertrophy in rats with experimental heart failure.
TLDR
It is suggested that Rho kinase-dependent pathways are involved in the mechanisms of renal vasoconstriction and cardiac hypertrophy in rats with volume-overload heart failure and selective blockade of these signaling pathways may be considered an additional tool to improve renal perfusion and attenuate cardiac hyperTrophy in heart failure. Expand
The Role of Rho Kinase in Sex-Dependent Vascular Dysfunction in Type 1 Diabetes
TLDR
Chronic treatment with fasudil increased contractions to serotonin in aorta from both non-diabetic and diabetic males, and long-term fAsudil treatment may increase compensatory mechanisms to enhance vasoconstrictions. Expand
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