Cell-specific impact of nitric oxide-dependent guanylyl cyclase on arteriogenesis and angiogenesis in mice

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• 作者：Noomen Bettaga ; Ronald J?ger ; Sarah Dünnes ; Dieter Groneberg…
• 关键词：Vasculature ; cGMP ; Ischemia ; Pericyte ; Signal transduction
• 刊名：Angiogenesis
• 出版年：2015
• 出版时间：July 2015
• 年：2015
• 卷：18
• 期：3
• 页码：245-254
• 全文大小：1,776 KB
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• 作者单位：Noomen Bettaga (1)
  Ronald J?ger (1)
  Sarah Dünnes (1)
  Dieter Groneberg (1)
  Andreas Friebe (1)
  
  1. Physiologisches Institut, Universit?t Würzburg, R?ntgenring 9, 97070, Würzburg, Germany
  
• 刊物类别：Medicine
• 刊物主题：Medicine & Public Health
  Oncology
  Cancer Research
  Cell Biology
  Cardiology
  Ophthalmology
  
• 出版者：Springer Netherlands
• ISSN：1573-7209

文摘

Nitric oxide (NO) acts as essential regulator of vasculogenesis and angiogenesis and is critical for arteriogenesis. Whether NO’s effects in vivo are mediated through NO-sensitive guanylyl cyclase (NO-GC) and thus by cGMP-dependent mechanisms has been only poorly addressed. Mice lacking NO-GC globally or specifically in smooth muscle cells (SMC) or endothelial cells (EC) were subjected to two established models for arteriogenesis and angiogenesis, namely hindlimb ischemia and oxygen-induced retinopathy. Our data clearly show the involvement of NO-GC in the recovery of blood flow after hindlimb ischemia, and this effect could be attributed to NO-GC in SMC. In the retina, global deletion of NO-GC led to reduced oxygen-induced vessel loss and hypoxia-induced capillary regrowth, whereas pathological neovascularization was increased. These effects were also seen in mice with SMC-specific NO-GC deletion but not in animals lacking NO-GC in EC. Intriguingly, NO-GC was found to be strongly expressed in retinal pericytes. Our data prove the involvement of NO-GC in growth and plasticity of hindlimb and retinal vasculature after ischemic/hypoxic insult.