Sinha Mithun, Ghatak Subhadip, Roy Sashwati, Sen Chandan K
Center for Regenerative Medicine and Cell Based Therapies, Davis Heart and Lung Research Institute, Ohio State University , Columbus, Ohio.
Antioxid Redox Signal. 2015 May 10;22(14):1257-72. doi: 10.1089/ars.2014.6065.
Angiogenesis is the process by which new blood vessels develop from a pre-existing vascular system. It is required for physiological processes such as developmental biology and wound healing. Angiogenesis also plays a crucial role in pathological conditions such as tumor progression. The underlying importance of angiogenesis necessitates a highly regulated process.
Recent works have demonstrated that the process of angiogenesis is regulated by small noncoding RNA molecules called microRNAs (miRs). These miRs, collectively referred to as angiomiRs, have been reported to have a profound effect on the process of angiogenesis by acting as either pro-angiogenic or anti-angiogenic regulators.
In this review, we will discuss the role of miR-200b as a regulator of angiogenesis. Once the process of angiogenesis is complete, anti-angiogenic miR-200b has been reported to provide necessary braking. Downregulation of miR-200b has been reported across various tumor types, as deregulated angiogenesis is necessary for tumor development. Transient downregulation of miR-200b in wounds drives wound angiogenesis.
New insights and understanding of the molecular mechanism of regulation of angiogenesis by miR-200b has opened new avenues of possible therapeutic interventions to treat angiogenesis-related patho-physiological conditions. Antioxid. Redox Signal. 22, 1257-1272.
血管生成是新血管从预先存在的血管系统发育而来的过程。它是发育生物学和伤口愈合等生理过程所必需的。血管生成在肿瘤进展等病理状况中也起着关键作用。血管生成的根本重要性需要一个高度受调控的过程。
最近的研究表明,血管生成过程受称为微小RNA(miR)的小非编码RNA分子调控。这些miR统称为血管生成miR,据报道它们通过作为促血管生成或抗血管生成调节因子对血管生成过程产生深远影响。
在本综述中,我们将讨论miR-200b作为血管生成调节因子的作用。一旦血管生成过程完成,据报道抗血管生成的miR-200b会提供必要的制动作用。在各种肿瘤类型中均有报道miR-200b表达下调,因为血管生成失调是肿瘤发展所必需的。伤口中miR-200b的短暂下调会促进伤口血管生成。
对miR-200b调节血管生成分子机制的新见解和理解为治疗血管生成相关病理生理状况开辟了新的可能治疗干预途径。《抗氧化与氧化还原信号》22卷,第1257 - 1272页。