microRNA-200b as a Switch for Inducible Adult Angiogenesis

被引:41
作者
Sinha, Mithun [1 ]
Ghatak, Subhadip [1 ]
Roy, Sashwati [1 ]
Sen, Chandan K. [1 ]
机构
[1] Ohio State Univ, Ctr Regenerat Med & Cell Based Therapies, Davis Heart & Lung Res Inst, Columbus, OH 43210 USA
基金
美国国家卫生研究院;
关键词
EPITHELIAL-MESENCHYMAL TRANSITION; RECEPTOR TYROSINE KINASE; SMOOTH-MUSCLE-CELLS; WILD-TYPE P53; ENDOTHELIAL-CELLS; TUMOR ANGIOGENESIS; IN-VIVO; SUPPRESSES ANGIOGENESIS; TRANSCRIPTIONAL CONTROL; WOUND ANGIOGENESIS;
D O I
10.1089/ars.2014.6065
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Significance: 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 Advances: 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. Critical Issues: 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. Future Directions: 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.
引用
收藏
页码:1257 / 1272
页数:16
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