Chengzhen Bao
Research Subjects
Research Interests
Chengzhen Bao has a total of 16 co-authors. Here are the top co-authors by number of shared publications:
- Bingying Fang
Advanced Institute for Medical Sciences, Dalian Medical University, Dalian 116041, China
1 shared publication - Feng Zheng
Health Science Center, East China Normal University, Shanghai, China
1 shared publication - Guangrui Yang
School of Clinical Medicine, Shanghai University of Medicine & Health Sciences, Shanghai, China
1 shared publication - Hu Xu
Health Science Center, East China Normal University, Shanghai, China
1 shared publication - Lan Ye
Advanced Institute for Medical Sciences, Dalian Medical University, Dalian 116041, China
1 shared publication - Lei Qian
Advanced Institute for Medical Sciences, Dalian Medical University, Dalian, China
1 shared publication
Latest Publications
- Open Access
- 9 July 2020
- Published by American Society for Clinical Investigation in JCI Insight
- Vol. 5 (13)
Endothelial cell prostaglandin E2 receptor EP4 is essential for blood pressure homeostasis
Prostaglandin E 2 and its cognate EP1–4 receptors play important roles in blood pressure (BP) regulation. Herein, we show that endothelial cell–specific (EC-specific) EP4 gene–knockout mice (EC-EP4 –/– ) exhibited elevated, while EC-specific EP4-overexpression mice (EC-hEP4 OE ) displayed reduced, BP levels compared with the control mice under both basal and high-salt diet–fed conditions. The altered BP was completely abolished by treatment with l– N G -nitro-l-arginine methyl ester (l-NAME), a competitive inhibitor of endothelial nitric oxide synthase (eNOS). The mesenteric arteries of the EC-EP4 –/– mice showed increased vasoconstrictive response to angiotensin II and reduced vasorelaxant response to acetylcholine, both of which were eliminated by l-NAME. Furthermore, EP4 activation significantly reduced BP levels in hypertensive rats. Mechanistically, EP4 deletion markedly decreased NO contents in blood vessels via reducing eNOS phosphorylation at Ser1177. EP4 enhanced NO production mainly through the AMPK pathway in cultured ECs. Collectively, our findings demonstrate that endothelial EP4 is essential for BP homeostasis.
- 9 July 2020
- Published by American Society for Clinical Investigation in JCI Insight
- Vol. 5 (13)
Open AccessEndothelial cell prostaglandin E2 receptor EP4 is essential for blood pressure homeostasis
Prostaglandin E 2 and its cognate EP1–4 receptors play important roles in blood pressure (BP) regulation. Herein, we show that endothelial cell–specific (EC-specific) EP4 gene–knockout mice (EC-EP4 –/– ) exhibited elevated, while EC-specific EP4-overexpression mice (EC-hEP4 OE ) displayed reduced, BP levels compared with the control mice under both basal and high-salt diet–fed conditions. The altered BP was completely abolished by treatment with l– N G -nitro-l-arginine methyl ester (l-NAME), a competitive inhibitor of endothelial nitric oxide synthase (eNOS). The mesenteric arteries of the EC-EP4 –/– mice showed increased vasoconstrictive response to angiotensin II and reduced vasorelaxant response to acetylcholine, both of which were eliminated by l-NAME. Furthermore, EP4 activation significantly reduced BP levels in hypertensive rats. Mechanistically, EP4 deletion markedly decreased NO contents in blood vessels via reducing eNOS phosphorylation at Ser1177. EP4 enhanced NO production mainly through the AMPK pathway in cultured ECs. Collectively, our findings demonstrate that endothelial EP4 is essential for BP homeostasis.