Involvement of RhoA/Rho-kinase in l-cysteine/H2S pathway-induced inhibition of agonist-mediated corpus cavernosal smooth muscle contraction

Nitric Oxide ◽  
2019 ◽  
Vol 85 ◽  
pp. 54-60 ◽  
Author(s):  
Fatma Aydinoglu ◽  
Elif Özveren Adıbelli ◽  
Didem Yılmaz-Oral ◽  
Nuran Ogulener
2004 ◽  
Vol 143 (4) ◽  
pp. 477-484 ◽  
Author(s):  
Dedmer Schaafsma ◽  
Reinoud Gosens ◽  
I Sophie T Bos ◽  
Herman Meurs ◽  
Johan Zaagsma ◽  
...  

2017 ◽  
Vol 5 (5) ◽  
pp. e00343 ◽  
Author(s):  
Ancy D. Nalli ◽  
Hongxia Wang ◽  
Sayak Bhattacharya ◽  
Bryan A. Blakeney ◽  
Karnam S. Murthy

2015 ◽  
Vol 93 (6) ◽  
pp. 405-411 ◽  
Author(s):  
Othman Al-Shboul ◽  
Ayman Mustafa

Recent studies have shown that both Rho kinase signaling and oxidative stress are involved in the pathogenesis of a number of human diseases, such as diabetes mellitus, hypertension, and atherosclerosis. However, very little is known about the effect of oxidative stress on the gastrointestinal (GI) smooth muscle Rho kinase pathway. The aim of the current study was to investigate the effect of oxidative stress on Rho kinase II and muscle contraction in rat stomach. The peroxynitrite donor 3-morpholinosydnonimine (SIN-1), hydrogen peroxide (H2O2), and peroxynitrite were used to induce oxidative stress. Rho kinase II expression and ACh-induced activity were measured in control and oxidant-treated cells via specifically designed enzyme-linked immunosorbent assay (ELISA) and activity assay kits, respectively. Single smooth muscle cell contraction was measured via scanning micrometry in the presence or absence of the Rho kinase blocker, Y-27632 dihydrochloride. All oxidant agents significantly increased ACh-induced Rho kinase II activity without affecting its expression level. Most important, oxidative stress induced by all three agents augmented ACh-stimulated muscle cell contraction, which was significantly inhibited by Y-27632. In conclusion, oxidative stress activates Rho kinase II and enhances contraction in rat gastric muscle, suggesting an important role in GI motility disorders associated with oxidative stress.


FEBS Letters ◽  
2000 ◽  
Vol 482 (1-2) ◽  
pp. 85-90 ◽  
Author(s):  
Natsuko Todoroki-Ikeda ◽  
Yoichi Mizukami ◽  
Kimiko Mogami ◽  
Takeshi Kusuda ◽  
Kuniko Yamamoto ◽  
...  

2006 ◽  
Vol 534 (1-3) ◽  
pp. 210-217 ◽  
Author(s):  
Teresa Quinn ◽  
Ronan Feighery ◽  
Alan William Baird

2009 ◽  
Vol 296 (4) ◽  
pp. H1048-H1057 ◽  
Author(s):  
Sachin A. Gupte ◽  
Pawel M. Kaminski ◽  
Shimran George ◽  
Lioubov Kouznestova ◽  
Susan C. Olson ◽  
...  

Protein kinase C (PKC) stimulation of NAD(P)H oxidases (Nox) is an important component of multiple vascular disease processes; however, the relationship between oxidase activation and the regulation of vascular smooth muscle contraction by PKC remains poorly understood. Therefore, we examined the signaling cascade of PKC-elicited Nox activation and the role of superoxide and hydrogen peroxide in mediating PKC-induced vascular contraction. Endothelium-denuded bovine coronary arteries showed a PKC-dependent basal production of lucigenin (5 μM)-detected Nox oxidase-derived superoxide, which was stimulated fourfold by PKC activation with 10 μM phorbol 12,13-dibutyrate (PDBu). PDBu appeared to increase superoxide generation by Nox2 through both p47phox and peroxide-dependent Src activation mechanisms based on the actions of inhibitors, properties of Src phosphorylation, and the loss of responses in aorta from mice deficient in Nox2 and p47phox. The actions of inhibitors of contractile regulating mechanisms, scavengers of superoxide and peroxide, and responses in knockout mouse aortas suggest that a major component of the contraction elicited by PDBu appeared to be mediated through peroxide derived from Nox2 activation stimulating force generation through Rho kinase and calmodulin kinase-II mechanisms. Superoxide generated by PDBu also attenuated relaxation to nitroglycerin. Peroxide-derived from Nox2 activation by PKC appeared to be a major contributor to the thromboxane A2 receptor agonist U46619 (100 nM)-elicited contraction of coronary arteries. Thus a p47phox and Src kinase activation of peroxide production by Nox2 appears to be an important contributor to vascular contractile mechanisms mediated through activation of PKC.


Sign in / Sign up

Export Citation Format

Share Document