Up-regulation of angiotensin-converting enzyme in response to acute ischemic stroke via ERK/NF-κB pathway in spontaneously hypertensive rats
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Zhou Ou1,*, Meng-Xing Tao1,*, Qing Gao1,*, Xue-Ling Zhang2, Yang Yang1, Jun-Shan Zhou1 and Ying-Dong Zhang1
1Department of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing, People’s Republic of China
2Department of Neurology, Suqian City People’s Hospital, Suqian, People’s Republic of China
Ying-Dong Zhang, email: Zhangyingdong@aliyun.com
Keywords: renin-angiotensin system, angiotensin-converting enzyme, mitogen-activated protein kinase, nuclear factor-κB, acute ischemic stroke
Received: June 22, 2017 Accepted: September 08, 2017 Published: September 22, 2017
Cerebral ischemic stroke is usually caused by a temporary or permanent decrease in blood supply to the brain. Despite general progress in diagnosis and treatment, the prognosis of stroke is still unsatisfactory, and more detailed potential mechanisms are needed to investigate underlying the pathological process. Here, we showed that serum angiotensin-converting enzyme (ACE) concentration was positively correlated with infarct volume after acute ischemic stroke (AIS). Moreover, using a permanent middle cerebral artery occlusion rat model, we indicated for the first time that increased ACE expression in response to AIS was regulated by the ERK/NF-κB pathway in peri-infarct regions. More importantly, we disclosed that angiotensin II type 1 receptors were implicated in up-regulation of ACE expression in peri-infarct regions. These findings offer insight into ACE expression and activity in response to stroke, and further our understanding of ACE mechanisms.
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