scholarly journals Defective endothelial nitric oxide synthase signaling is mediated by rho-kinase activation in rats with secondary biliary cirrhosis

Hepatology ◽  
2007 ◽  
Vol 47 (3) ◽  
pp. 966-977 ◽  
Author(s):  
Go Anegawa ◽  
Hirofumi Kawanaka ◽  
Daisuke Yoshida ◽  
Kozo Konishi ◽  
Shohei Yamaguchi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Rho Kinase ◽  
Biliary Cirrhosis ◽  
Kinase Activation ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Secondary Biliary Cirrhosis

scholarly journals Functional Deterioration of Endothelial Nitric Oxide Synthase after Focal Cerebral Ischemia

2013 ◽  
Vol 33 (10) ◽  
pp. 1532-1539 ◽  
Author(s):  
Yoshiki Yagita ◽  
Kazuo Kitagawa ◽  
Naoki Oyama ◽  
Toshiro Yukami ◽  
Akihiro Watanabe ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cerebral Ischemia ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Focal Cerebral Ischemia ◽  
Rho Kinase ◽  
Ischemic Lesion ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Functional Deterioration

Endothelial nitric oxide synthase (eNOS) dysfunction is related to secondary injury and lesion expansion after cerebral ischemia. To date, there are few reports about postischemic alterations in the eNOS regulatory system. The purpose of the present study was to clarify eNOS expression, Ser1177 phosphorylation, and monomer formation after cerebral ischemia. Male Wistar rats were subjected to transient focal cerebral ischemia. Endothelial nitric oxide synthase messenger RNA (mRNA) and protein expression increased ~ 8-fold in the ischemic lesion. In the middle cerebral artery core, eNOS-Ser1177 phosphorylation increased 6 hours after ischemia; however, there was an approximately 90% decrease in eNOS-Ser1177 phosphorylation observed 24 hours after ischemia that continued until at least 7 days after ischemia. Endothelial nitric oxide synthase monomer formation also increased 24 and 48 hours after ischemia ( P<0.05), and protein nitration progressed in parallel with monomerization. To assess the effect of a neuroprotective agent on eNOS dysfunction, we evaluated the effect of fasudil, a Rho-kinase inhibitor, on eNOS phosphorylation and dimerization. Postischemic treatment with fasudil suppressed lesion expansion and dephosphorylation and monomer formation of eNOS. In conclusion, functional deterioration of eNOS progressed after cerebral ischemia. Rho-kinase inhibitors can reduce ischemic lesion expansion as well as eNOS dysfunction in the ischemic brain.

scholarly journals 404-3 Dual regulation of endothelial nitric oxide synthase by Rho-kinase

2004 ◽  
Vol 43 (5) ◽  
pp. A532
Author(s):  
Yoshiyuki Rikatake ◽  
Rosario Scalia ◽  
Michael A Moskowitz ◽  
James K Liao
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Rho Kinase ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide
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