Endothelial nitric oxide synthase in red blood cells: key to a new erythrocrine function?
Endothelial nitric oxide synthase in red blood cells: key to a new erythrocrine function?
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DOI:
10.1016/j.redox.2013.12.027
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发表时间:
2014
期刊:
影响因子:
11.4
通讯作者:
Kelm M
中科院分区:
文献类型:
--
作者:
Cortese-Krott MM;Kelm M
Red blood cells (RBC) have been considered almost exclusively as a transporter of metabolic gases and nutrients for the tissues. It is an accepted dogma that RBCs take up and inactivate endothelium-derived NO via rapid reaction with oxyhemoglobin to form methemoglobin and nitrate, thereby limiting NO available for vasodilatation. Yet it has also been shown that RBCs not only act as “NO sinks”, but exert an erythrocrine function – i.e an endocrine function of RBC – by synthesizing, transporting and releasing NO metabolic products and ATP, thereby potentially controlling systemic NO bioavailability and vascular tone. Recent work from our and others laboratory demonstrated that human RBCs carry an active type 3, endothelial NO synthase (eNOS), constitutively producing NO under normoxic conditions, the activity of which is compromised in patients with coronary artery disease. In this review we aim to discuss the potential role of red cell eNOS in RBC signaling and function, and to critically revise evidence to this date showing a role of non-endothelial circulating eNOS in cardiovascular pathophysiology. We define erythrocrine function the ability of RBC to secret signaling entities or transmitter momlecules. Erythocrine function include scavenging, transporting and producing NO metabolites and ATP. There is in vitro and in vivo evidence of a role of red cell eNOS in signaling and erythrocrine function. Red cell eNOS and erythocrine function might be involved in organ protection. Further studies should address the role of red cell eNOS/RBC signaling in cardiovascular health.