Regular ArticleActivation of Rho Is Involved in the Mechanism of Hydrogen-Peroxide-Induced Lung Edema in Isolated Perfused Rabbit Lung
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Association of Rho-kinase Gene Polymorphisms with Respiratory Distress Syndrome in Preterm Neonates
2017, Pediatrics and NeonatologyCitation Excerpt :There is evidence that the Rho/ROCK pathway plays an important role as mechanosensor acting in vivo either directly or indirectly for transforming increased distention into acceleration of lung growth.14 In experimental studies, systemic administration of a ROCK inhibitor, Y-27632, substantially reduced pulmonary microvascular permeability, edema, and lung injury.15,16 ROCK may play an important role in the pathogenesis of lipopolysaccharide-induced lung injury; and ROCK inhibition could attenuate cytoskeletal rearrangement of endothelial cells, leading to decreased neutrophil emigration into the lung parenchyma.17
Sepsis-induced leukocyte adhesion in the pulmonary microvasculature in vivo is mediated by CD11a and CD11b
2013, European Journal of PharmacologyAssociation between Rho-kinase (ROCK2) gene polymorphisms and Behçet's disease
2012, Translational ResearchVascular hyperpermeability in response to inflammatory mustard oil is mediated by Rho kinase in mice systemically exposed to arsenic
2011, Microvascular ResearchCitation Excerpt :Myosin phosphatase target protein (MYPT1) is a subunit of MLCP and a downstream target protein of Rho kinase (ROCK) following RhoA activation. It has been established that activation of the Rho/ROCK pathway leads to the inactivation of MLCP, which prevents dephosphorylation of MLC, resulting in increased endothelial contractility (Adamson et al., 2002; Chiba et al., 2001; Hirase et al., 2001; Wang et al., 2001). It is known that ROCK is involved in the barrier dysfunction of cultured endothelial cells subjected to thrombin (Birukova et al., 2004), VEGF (Sun et al., 2006) and TNF-α (Tasaka et al., 2005).
ROCK induced inflammation of the microcirculation during endotoxemia mediated by nitric oxide synthase
2011, Microvascular ResearchCitation Excerpt :This is in agreement with published in vitro studies, investigating the timing of Rho activation (Essler et al., 2000). Ex vivo experimentation in rabbit lung has also demonstrated that preventing ROCK inhibition down-regulates hydrogen peroxide-induced leak responses (Chiba et al., 2001). However, this current in vivo study is the first to investigate Rho/ROCK activation following an inflammatory stimulus such as LPS application between 0 and 4 h.
Long-term cyclic stretch controls pulmonary endothelial permeability at translational and post-translational levels
2008, Experimental Cell Research
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To whom correspondence should be addressed at Department of Pulmonary Medicine and Clinical Immunology, Dokkyo University School of Medicine, 880 Kitakobayashi, Mibu, Tochigi 321-0293, Japan. Fax:+81-282-86-5080. E-mail: [email protected].